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83 publications mentioning hsa-mir-296

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-296. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 446
Antagonizing DNA methylation using 5-aza-2'-deoxycytidine caused an efficient up-regulation of mature miR-296-5p and miR-512-5p in MDA-MB-231 cells that was enhanced when 5-aza-2'-deoxycytidine was combined with HDAC inhibitors: miR-296-5 pexpression was increased upon TSA treatment, a reported inhibitor of class I and II HDACs; in contrast, miR-512-5p was increased upon treatment with the pan-class I and II HDAC inhibitor Vorinostat (SAHA). [score:12]
Altogether our data suggest a mo del where epigenetic silencing of miR-296-5p and miR-512-5p expression in basal breast cancer cells releases hTERT expression from miRNA mediated suppression of gene expression. [score:9]
However, given the complexity of hTERT gene expression control and the numerous mRNAs targeted by miR-296-5p and miR-512-5p, we cannot completely exclude that indirect effects contribute to miR-296-5p and miR-512-5p dependent control of hTERT expression. [score:8]
Altogether our data suggest that low miR-512-5p and miR-296-5p expression may have a role in assisting the establishment of a gene expression signature that includes hTERT upregulation, and contributes to the aggressiveness of basal type breast cancer. [score:8]
Poor survival of basal type breast cancer with high hTERT expression appears to be recapitulated in specimen with enhanced expression of validated miR-296-5p or miR-512-5p target genes, including hTERT. [score:7]
miR-296-5p has been shown to suppress cancer progression, metastasis, and neo-vascularization by targeting the expression of multiple genes including HMGA1, PUMA and SCRIB [35, 37, 54]. [score:7]
Rescue experiments in breast cancer cells expressing hTERT lacking the 3’UTR revealed that this proliferation defects can be directly attributed to miR-296-5p and miR-512-5p dependent down-regulation of hTERT. [score:7]
This might provide first evidence that downregualtion of miR-296-5p, miR-512-5p in basal type breast cancer might help to promote the expression of a set of target genes, that could contribute to the aggressiveness of basal type breast cancer and hTERT expression in basal type breast cancer. [score:7]
Gene expression analyses suggest that high expression of hTERT and a panel of cancer relevant miR-296-5p and miR-512-5p target genes appear to be linked with reduced distant metastasis free survival and relapse free survival of basal breast cancer patients. [score:7]
We next used public gene expression datasets to test whether the expression of validated miR-296-5p or miR-512-5p target genes may have a special relevance in basal type breast cancer. [score:7]
The observation of reduced distant metastasis free survival and relapse free survival of basal type breast cancer patients with increased miR-296-5p and miR-512-5p target gene expression signatures suggest that epigenetic regulation of miR-296 and miR-512 may be of relevance in this breast cancer subtype. [score:6]
miR-296-5p and miR-512-5p act as negative regulators of telomerase activity and telomere length by targeting hTERT expression. [score:6]
miR-512-5p and miR-296-5p regulate telomere homeostasis by targeting hTERT expression. [score:6]
Disrupting miRNA gene silencing by the use of epigenetic drugs causes a dramatic miR-296-5p and miR-512-5p upregulation and concomitant reduction of hTERT expression that reduces the resistance to apoptotic stimuli. [score:6]
We consequently wished to test whether miR-296-5p and miR-512-5p are critical components that down-regulate hTERT expression in basal type breast cancer cells that are treated with epigenetic drugs. [score:6]
In addition, we confirmed down-regulation of previously reported miR-296-5p targets IKBKE and PUMA (BBC3) in mimic-miR-296-5p transfected MDA-MB-231 cells (Supplementary Figure 6A-6E). [score:6]
However, given the fact that multiple pathways impinge on telomerase expression, indirect effects triggered miR-296-5p or miR-512-5p on altered hTERT expression cannot be completely excluded. [score:6]
miR-296-5p and miR-512-5p target the 3’UTR of hTERT and are down-regulated in breast cancer. [score:6]
Low expression of miR-296-5p and miR-512-5p in breast cancer indicates that miR-296 and miR-512 hosting gene expression is tightly regulated. [score:6]
Recently, miR-512-5p has been shown to modulate the expression of the apoptosis regulator MCL-1, and miR-296-5p has been demonstrated to reduce cell proliferation of breast and prostate cancer cells by targeting SCRIB or HMGA1, respectively [35, 36, 42]. [score:6]
Future efforts should aim to use a large set of specimen obtained from basal type breast cancer in order to experimentally validate the link between epigenetic silencing of miR-296 and miR-512, increased expression of validated miR-296-5p/miR-512-5p target genes and telomere homeostasis in a clinical setting. [score:5]
Real-time PCR analysis revealed that TSA or SAHA treatment does not significantly impact on the expression of HDACs, suggesting that observed alteration in miR-296-5p and miR-512-5p are not triggered via altered HDAC expression (Supplementary Figure 9A-9J). [score:5]
Ectopic hTERT expression rescues proliferation, DNA damage and apoptosis marker expression triggered by miR-296-5p or miR-512-5p. [score:5]
Cancer specimens with high expression of miR-296-5p target genes, previously validated in MDA-MB-231 cells, show poor survival. [score:5]
Treatment of MDA-MB-231 cells with the HDAC inhibitors trichostatin (TSA) or Vorinostat (suberoylanilide hydroxamic acid, SAHA) increased miR-296-5p expression levels 4 fold or 5 fold, respectively (Figure 5C). [score:5]
Epigenetic silencing of miR-296 and miR-512 genes in basal type breast cancer cells releases hTERT from miRNA dependent suppression of gene expression. [score:5]
We next set out to investigate whether hTERT expression and miR-296-5p or miR-512-5p target gene expression signatures impact on clinical parameters of defined subtypes of breast cancer. [score:5]
Altered expression of miR-296-5p target genes does not impact on patient survival of other breast cancer subtypes (data not shown). [score:5]
Figure 6 Epigenetic silencing of miR-296 and miR-512 genes in basal type breast cancer cells releases hTERT from miRNA dependent suppression of gene expression. [score:5]
Increased hTERT and miR-296-5p/miR-512-5p target gene expression is linked to poor clinical outcome in basal type breast cancer. [score:5]
Together, these data show that low expression of miR-296-5p and miR-512-5p ensures elevated hTERT expression to improve cell proliferation potential. [score:5]
Performing a series of gain and loss of function experiments we show that miR-296-5p and miR-512-5p have a relevant role in the direct regulation of hTERT expression in two different human breast cancer cell lines. [score:5]
The 3’UTR of hTERT contains 3 predicted target sites for miR-296-5p and one target site for miR-512-5p (Figure 1D, 1J). [score:5]
In line with this, stable expression of a miR-296-5p or miR-512-5p precursor stemloop construct in MDA-MB-231 basal type breast cancer cells, resulted in a significant reduction of hTERT expression and telomerase activity after approximately 18 population doublings. [score:5]
Introduction of antagomiR-296-5p or antagomiR-512-5p that target endogenous mature miR-296-5p or miR-512-5p, resulted in a significant increase of hTERT mRNA expression levels in both, MCF-7 and MDA-MB-231 cells (Figure 2B, 2D). [score:5]
As expected, treatment with the DNMT inhibitor 5-aza-2'-deoxycytidine reduced DNA methylation levels of CpG rich regions of interest and mediated a 5 fold or 70 fold increase of miR-296-5p or miR-512-5p expression levels, respectively (Figure 5A, 5B). [score:5]
Figure 5 (A) miR-296-5p expression upon inhibition of DNA methylation as determined by quantitative TaqMan RT-PCR. [score:5]
We found that the expression of miR-296-5p target genes hTERT, HMGA1, MMP1, MAP2K3, SCRIB, PUMA (BBC3) and IKBKE is higher in basal breast cancer and linked with significantly reduced distant metastasis free survival and relapse free survival in pooled breast cancer subtypes and basal type breast cancer (Figure 3D, 3F). [score:5]
Together, this gives strong evidence that in breast cancer cells hTERT expression levels is directly controlled by miR-296-5p and miR-512-5p dosage. [score:4]
In accordance with hTERT mRNA expression data we found that ectopic introduction of miR-296-5p or miR-512-5p resulted in a significant reduction of overall telomerase activity in MCF-7 cells; this result was recapitulated by siRNA mediated knock down of hTERT (Figure 2E-2F). [score:4]
Together, this demonstrates that miR-296-5p and miR-512-5p have a central role in executing epigenetic regulatory circuits that control hTERT expression and telomere length in cancer cells. [score:4]
This suggests that direct targeting of the hTERT 3’UTR by miR-512-5p or miR-296-5p has a major contribution to the observed proliferation defects. [score:4]
Expression analysis revealed that miR-296-5p expression levels are dramatically reduced in a panel of basal type breast cancer cell lines including MDA-MB-231, MDA-MB-468 and MDA-MB-157 when compared to luminal type breast cell lines MCF-7, SK-BR3 or T-47D (Figure 3J). [score:4]
This suggests that miR-512-5p and miR-296-5p act as potent tumor suppressive miRNAs that exert their anti-proliferative function along multiple pathways that include the regulation of hTERT, the catalytic subunit of the telomerase complex. [score:4]
DNA methylation analysis focused on CpG islands located in vicinity to the miRNA hosting genes, but also on CpG islands with a reported role in regulating miR-296-5p and miR-512-5p expression [37][42]. [score:4]
This data is supported by down-regulation of miR-296-5p and miR-512-5p in basal type human breast cancer (Figure 1C). [score:4]
This demonstrates that epigenetic regulation of miR-296-5p and miR-512-5p impacts on hTERT expression levels in basal type breast cancer cells. [score:4]
Out of this panel, miR-296-5p and miR-512-5p are significantly down-regulated in human breast cancer specimen. [score:4]
Together, this indicates that miR-296-5p and miR-512-5p are regulators of telomerase expression that impact on telomerase activity and telomere homeostasis in breast cancer cells. [score:4]
These data support evidence for a link between miR-296-5p and miR-512-5p and the regulation of hTERT expression. [score:4]
This underlines that down-regulation of miR-296-5p represents a general feature of basal-type breast cancer cells. [score:4]
Together, these data may provide indications that miR-296-5p and miR-512-5p dependent regulation of hTERT is part of a miR-296-5p/miR-512-5p target gene signature that contributes to poor clinical outcome in basal type breast cancer. [score:4]
Ectopic introduction of mimic-miR-296-5p or mimic-miR-512-5p in MCF-7 luminal type or MDA-MB-231 basal type breast cancer cells caused an approximately 70% or 30% reduction of endogenous hTERT mRNA expression levels, respectively (Figure 2A, 2C). [score:3]
Low miR-296-5p and miR-512-5p expression levels in basal type breast cancer cell lines suggest that the respective miR-296, miR-512-1 and miR-512-2 genes might be subjected to efficient repression or gene silencing. [score:3]
In line with this, targeting of endogenous miR-296-5p or miR-512-5p using antagomiRs increased cell proliferation rates (Figure 4A). [score:3]
The interplay between epigenetic gene silencing and miR-296/miR-512 to favor hTERT expression identifies basal type breast cancer as potential breast cancer subtype to explore telomerase related therapeutic approaches. [score:3]
We found that Hela cells transiently transfected with hTERT 3’UTR luciferase reporters carrying mutations in individual target sites for miR-296-5p or miR-512-5p show increased luciferase reporter activity when compared to cells transfected with a wild type 3’UTR luciferase reporter (Supplementary Figure 2C, 2D). [score:3]
In line with this, we observed telomere shortening in cells overexpressing mature miR-296-5p or miR-512-5p. [score:3]
This is consistent with the requirement of telomerase expression in cancer cells and anticipates clinical relevance for miR-296-5p and miR-512-5p. [score:3]
In particular, miR-296-5p was demonstrated to have a tumor suppressive role in breast, prostate, non-small cell lung cancer or glioblastoma [35– 40]. [score:3]
To validate the specificity of miR-296-5p and miR-512-5p for the 3’UTR of hTERT we generated hTERT 3’UTR luciferase reporter constructs that contain deletions of the individual miR-296-5p or miR-512-5p target sites (Figure 1D, 1J). [score:3]
Epigenetic silencing of miR-296-5p and miR-512-5p ensures hTERT expression in basal-type breast cancer cells. [score:3]
We next validated that impaired proliferation of miR-296-5p or miR-512-5p transfected MDA-MB-231 basal type breast cancer cells is due to reduced hTERT expression. [score:3]
Remarkably, the extremely short hTERT 3’UTR in rodents does not contain miR-296-5p and miR-512-5p target sites (data not shown). [score:3]
J, K. : 3 independent experiments were carried out, error bars indicate statistical significance; to better visualize differences in miR-296-5p and miR-512-5p, respective expression levels were set “1” in MDA-MB-468 cells. [score:3]
In particular, our data suggest that DNA methylation and histone de-acetylation collaborate as redundant epigenetic mechanisms to silence the expression of miR-296-5p and miR-512-5p in basal type breast cancer cells. [score:3]
Functional validation revealed that miR-296-5p and miR-512-5p target specific sites in the 3’UTR of hTERT. [score:3]
Along these lines, the exploration of epigenetic inhibitors in more complex preclinical mo dels could provide valuable insights into the relevance of miR-296 and miR-512 in imposing an anti-tumor effect that includes telomere related pathways in basal type breast cancer. [score:3]
We next wished to demonstrate that miR-296-5p and miR-512-5p impact on hTERT expression in classic breast cancer mo del cell lines. [score:3]
This highlights that DNA methylation and histone de-acetylation collaborate to silence miR-296-5p and miR-512-5p in basal type breast cancer cells to ensure increased hTERT expression, thus resulting in improved protection from apoptosis. [score:3]
A similar trend for miR-296-5p and miR-512-5p target genes was found in the GOBO dataset (Supplementary Figure 6F-6H; Supplementary Figure 7I-7K)[45]. [score:3]
miR-296-5p–hTERT target sites are conserved in humans, chimpanzee and rhesus monkeys (Supplementary Figure 2B). [score:3]
Together, these data demonstrate target specificity of miR-296-5p and miR-512-5p for the 3’UTR of hTERT. [score:3]
Importantly, we found that ectopic expression of hTERT rescues miR-296-5p or miR-512-5p induced cell proliferation defects (Figure 4D and 4E). [score:3]
Performing gain and loss of function experiments we found that hTERT expression and telomerase activity is under control of both, miR-296-5p and miR-512-5p. [score:3]
This suggests that miR-296-5p and miR-512-5p execute epigenetic programs that control hTERT expression in breast cancer cells. [score:3]
Mutations of miR-296-5p target sites result in increased luciferase reporter activity, when compared to the hTERT wild-type 3’UTR reporter constructs. [score:3]
Altogether, our data suggest that silencing of miR-296-5p and miR-512-5p in basal type breast cancer helps to establish high hTERT expression levels, and may contribute to basal type breast cancer aggressiveness and reduced patient survival. [score:3]
A series of luciferase reporter experiments were carried out in HeLa and MDA-MB-231 basal type breast cancer cells that display comparable expression levels of endogenous miR-296-5p or miR-512-5p, respectively (Supplementary Figure 3A-3B). [score:3]
To achieve this, we antagonized TSA induced expression of miR-296 by transfecting MDA-MB-231 cells with antagomiR-296-5p and subsequently measured hTERT expression by RT-PCR. [score:3]
In our screen we identified miR-296-5p as novel hTERT -targeting miRNA. [score:3]
Performing a high-throughput luciferase reporter screen we show that miR-296-5p and miR-512-5p efficiently target the 3’UTR of hTERT. [score:3]
We treated MDA-MB-231 cells with DNA methyltransferase and histone deacetylase inhibitors and measured mature miR-512-5p and miR-296-5p expression levels by classic Taq-man PCR. [score:3]
Recent studies demonstrate targeting of HMGA1, MMP1, MAP2K3 and SCRIB by miR-296-5p in MDA-MB-231 cells [35, 36]. [score:3]
Bottom left panel, miR-296-5p expression in MDA-MB-231 cells treated with increasing concentrations of 5-aza-2’-deoxycytidine (5-aza). [score:3]
Deleting individual miR-296-5p target sites present in the 3’UTR of hTERT renders the hTERT 3’UTR luciferase reporter resistant to ectopically increased miR-296-5p levels (Figure 1F-1H, Supplementary Figure 3D-3F). [score:3]
Figure 2 (A, C) Transient transfection of MCF-7 (A) or MDA-MB-231 (C) cells with hTERT specific siRNAs or miR-296-5p or miR-512-5p mimics causes a reduction of hTERT mRNA expression as determined by quantitative RT-PCR. [score:3]
miR-296-5p and miR-512-5p suppress hTERT -mediated protection from apoptosis and senescence in basal type breast cancer cells. [score:3]
This suggests that TSA/SAHA treatment increases miR-296-5p and miR-512-5p levels, resulting in reduced hTERT expression. [score:3]
In line with this, ectopic hTERT reduced p21 expression in miR-296-5p transfected cells and reduced γH2AX levels as well as PARP and Caspase 3 cleavage in miR-296-5p or miR-512-5p transfected cells (Figure 4F). [score:3]
This prompted us to test whether epigenetic silencing of the miR-296-5p or miR-512-1 and miR-512-2 gene loci is aimed to ensure high hTERT expression. [score:3]
Importantly, due to dramatic differences of hTERT 3’UTR size and sequence content across vertebrate, targeting of hTERT by miR-296-5p and miR-512-5p is limited to human, chimpanzee and rhesus monkey. [score:3]
We therefore focused our further study on the functional relevance of miR-296-5p and miR-512-5p in controlling hTERT expression in human breast cancer. [score:3]
Consistent with an overall decrease in telomere length we found that the frequency of short telomeres increases whereas the frequency of long telomeres decreases in miR-296-5p or miR-512-5p overexpressing MDA-MB-231 cells (Supplementary Figure 4D). [score:3]
We found that among candidate miRNAs that mediate at least 50% reduction of hTERT 3’UTR reporter activity, only miR-296-5p, miR-512-5p and miR-1207-5p showed significant down-regulation in breast cancer when compared to healthy tissue (Figure 1A, 1C, Supplementary Figure 2A). [score:3]
Remarkably, human mammary epithelial cells display increased miR-296-5p expression levels compared to basal type breast cancer cells (Supplementary Figure 7L). [score:2]
miR-296 CpG-1 island (1751bp upstream of miR-296): Fw: 5’-GTGAAAGTAAGTTTTATTGATGGT-3’; Rv_ 5’-CAAAAAATTCCAAAAACCCTTAAA-3’, [37]; miR-296 CpG-2 island (88bp downstream of miR-296) : Fw: 5’-GTGTTAGGAGTGGAGATAGGATAGT-3’; Rv: 5’-TCAATAAAAATAAAAAAAACCTCC-3’; miR-512- CpG-1 island (2806bp upstream of miR-512-1): Fw: 5’-TTGTAATTTTAGTATTTTGGGAGGT-3’; Rv: 5’-AAAACAATCTCACTCTATTACCCAAAC-3’; miR-512 CpG-2 island, regulating the C19MC cluster (17692 bp upstream of miR-512-1) Fw_5’-TTTTTTTTGAGGGATTAGAATTTGTT-3’ RV_5’-CCCTAAACTTCCTAATTAAATAAAAAACTA-3’ PCR products were gel purified and cloned into pCR2.1 using the TA cloning kit (Invitrogen). [score:2]
In line with this, miR-296-5p and miR-512-5p have an anti-proliferative function in MCF-7 cells (Supplementary Figure 8E). [score:1]
We further show that miR-296 and miR-512 gene loci are subjected to gene silencing in basal type breast cancer cells. [score:1]
Ectopic introduction of miR-296-5p in MDA-MB-231 cells mediates increased p21 protein levels, modest PARP cleavage, as well as increased numbers of beta-galactosidase positive cells (Figure 4C; Supplementary Figure 8A). [score:1]
miR-512-5p and miR-296-5p have a reported role in various aspects of human cancer. [score:1]
Figure 4 (A) Cumulative cell numbers of MDA-MB-231 cells transiently transfected with miRNA control, miR-296-5p or miR-512-5p mimics. [score:1]
Top panel, Positions of CpG islands analyzed for the miR-296 locus. [score:1]
Epigenetic silencing of miR-296-5p and miR-512-5p protects MDA-MB-231 cells from apoptosis. [score:1]
miR-296-5p levels were quantified against RNU49. [score:1]
This indicates that miR-296-5p promotes cellular senescence but also supports a modest activation of apoptosis programs. [score:1]
miR-296-5p and miR-512-5p cause hTERT dependent cell proliferation defects in MDA-MB-231 basal type breast cancer cells. [score:1]
Numbers indicate distance from miR-296. [score:1]
In line with gain of function experiments, competing endogenous miR-296-5p or miR-512-5p by transfecting MDA-MB-231 cells with antagomiR siRNAs increased hTERT 3’UTR luciferase activity (Supplementary Figure 3I). [score:1]
In order to test the impact of miR-296-5p and miR-512-5p on cell proliferation we determined cumulative cell numbers of MDA-MB-231 basal type breast cancer cells with altered miR-296-5p and miR-512-5p levels. [score:1]
Ectopic miR-296-5p and miR-512-5p reduce telomerase activity, impair telomere maintenance and promote senescence and apoptosis in basal breast cancer cells. [score:1]
Cell cycle revealed that introduction of synthetic miR-296-5p siRNAs caused increased cell numbers in G1 phase and reduced cell numbers in S and G2/M phase, indicative for a G1-S phase arrest (Figure 4B). [score:1]
miR-296-5p and miR-512-5p contribute to poor survival. [score:1]
miR-296-5p is encoded by the lincRNA Nespas that is transcribed from parental allele of the imprinted GNAS cluster located at chromosome 20q13.3 [53]. [score:1]
Using a basal type breast cancer cell line, we show that increasing intracellular levels of mature miR-296-5p and miR-512-5p resulted in telomere shortening as well as induction of senescence and apoptosis, finally causing reduced cell proliferation. [score:1]
miR-296-5p and miR-512-5p reduce cell proliferation. [score:1]
Of notice, ectopic introduction of miR-296-5p in MDA-MB-231 cells did not alter miR-512-5p levels; altered miR-512-5p levels did not change miR-296-5p levels. [score:1]
ΔCt values (Ct miR-296-5p – Ct RNU49) are indicated. [score:1]
We found that ectopic introduction of synthetic miR-296-5p or miR-512-5p causes a significant reduction of MDA-MB-231 cell proliferation (Figure 4A). [score:1]
A mo del for miR-296-5p and miR-512-5p function in basal-type breast cancer. [score:1]
This suggests that different HDACs collaborate with DNMTs to ensure efficient epigenetic silencing of miR-296 or miR-512. [score:1]
Analogous data were obtained using p53 proficient MCF-7 luminal breast cancer cells: introducing miR-296-5p mimics into luminal MCF-7 cells activated senescence and apoptosis pathways; ectopic miR-512-5p exclusively activated apoptosis (Supplementary Figure 8C, 8D). [score:1]
To test whether miR-296-5p or miR-512-5p dependent reduction of hTERT mRNA levels is paralleled by a reduction of telomerase activity we performed TRAP analysis. [score:1]
Similar to miR-512-5p, we show that a 5-fold increase of miR-296-5p in 5-aza-2'-deoxycytidine treated MDA-MD-231 cells increased to 32-fold or 42 fold when 5-aza-2'-deoxycytidine was used in combination with TSA or SAHA, respectively (Figure 5F). [score:1]
Together, this indicates that repression of miR-296-5p and miR-512-5p in basal type breast cancer cells releases hTERT from miRNA dependent repression, to enhance resistance to apoptosis and telomere maintenance, thus promoting cancer cell aggressiveness. [score:1]
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[+] score: 436
Since miRNAs usually have multiple targets, further experiments were performed to check whether the cell mobility will be further inhibited or not after over -expression of miR-296 in S100A4 knockdown cells. [score:8]
b Immunofluorescence showed miR-296 overexpression increased E-cadherin expression and decreased Vimentin expression in HT29 cells. [score:7]
And the immunostaining accordingly showed that miR-296 overexpression evidently increased E-cadherin expression and decreased Vimentin expresssion (Fig.   4b). [score:7]
a showed overexpression of miR-296 decreased S100A4 and Vimentin expression, and increased E-cadherin expression in HT29 cells. [score:7]
Our data showed that overexpression of miR-296 could inhibit EMT of CRC cells while inhibition of miR-296 promoted EMT of CRC cells. [score:7]
And immunofluorescence data showed that E-cadherin expression was decreased while Vimentin expression was increased after miR-296 knockdown (Fig.   4d). [score:6]
d Immunofluorescence showed knockdown of miR-296 decreased E-cadherin expression and increased Vimentin expression in SW480 cells To further confirm that miR-296 could modulate EMT phenotype of CRC, IHC was performed in CRC tissues for S100A4, E-cadherin and Vimentin. [score:6]
Ectopic expression of miR-296 in HT29 cells prominently inhibits the migration and invasion of tumor cells, while miR-296 knockdown increased these behaviors of SW480 cells. [score:6]
c and d Compared with those of high miR-296 level (n = 45), miR-296 low -expressing patients (n = 45) had significantly reduced overall survival and recurrence-free survival To clarify the clinical value of miR-296 in CRC, all patients were grouped into miR-296 low and high expression groups according to the median expression of miR-296. [score:6]
d Immunofluorescence showed knockdown of miR-296 decreased E-cadherin expression and increased Vimentin expression in SW480 cells To further confirm that miR-296 could modulate EMT phenotype of CRC, IHC was performed in CRC tissues for S100A4, E-cadherin and Vimentin. [score:6]
S100A4 knockdown inhibited the migration and invasion of miR-296 underexpressing SW480 cells. [score:6]
Furthermore, we found that restoration of S100A4 reversed the anti-metastatic effects of miR-296 overexpression and S100A4 knockdown abrogate the effects of miR-296 inhibition on EMT and metastasis of CRC cells. [score:6]
c showed knockdown of miR-296 increased S100A4 and Vimentin expression, and decreased E-cadherin expression in SW480 cells. [score:6]
S100A4, a marker of EMT phenotype [23] and also a critical regulator of cancer growth and metastasis [24, 25], was recognized as a potential target molecule of miR-296, because the complementary sequence of miR-296 was identified in the 3’-UTR of S100A4 mRNA by TargetScan analysis. [score:6]
Our data indicated that miR-296 overexpression slightly reduced the number of migrated and invaded S100A4 knockdown HT29 cells without statistical significance (Additional file 1: Figure S1), suggesting that S100A4 was the major functional target of miR-296. [score:6]
As shown in Fig.   7a, S100A4 retroviruses infection significantly increased the levels of S100A4 and Vimentin while reduced E-cadherin expression in miR-296 overexpressing HT29 cells. [score:5]
Altogether, miR-296 exerts its inhibitory effects on CRC metastasis mainly by targeting S100A4. [score:5]
The Cox-regression analysis showed that lymph node status, distant metastasis, TNM stage and miR-296 expression were independent factors for the overall survival and disease free survival of CRC patients (P < 0.05, respectively, Table  2). [score:5]
Overexpression of miR-296 decreased the luciferase activity of wt 3’-UTR of S100A4 (P < 0.05, Fig.   6b) while inhibition of miR-296 increased the luciferase activity of wt 3’-UTR of S100A4 (P < 0.05, Fig.   6b). [score:5]
Therefore, these data indicate miR-296 can regulate the expression of S100A4 by directly interacting with its 3’-UTR in CRC. [score:5]
Taken together, these data demonstrate that miR-296 can suppress the metastasis of CRC cells by inhibiting EMT. [score:5]
In this study, we found that miR-296 could inhibit the expression of S100A4 in CRC cells. [score:5]
a SW480 cells that were transduced with negative control inhibitors (NC) or miR-296 inhibitors (anti-miR-296) were confirmed by qRT-PCR. [score:5]
And the expression of S100A4 in CRC tissues was negatively correlated with the expression level of miR-296. [score:5]
On the other hand, miR-296 silencing in SW-480 cells prominently decreased E-cadherin expression, and increased Vimentin and S100A4 expression (Fig.   4c). [score:5]
b Overexpression of miR-296 decreased while inhibition of miR-296 increased the luciferase activity of wt 3’-UTR of S100A4. [score:5]
S100A4 siRNA significantly decreased S100A4 in miR-296 silenced SW480 cells, and led to increased E-cadherin expression and decreased Vimentin expression. [score:5]
And miR-296 played a suppressive role in glioblastoma by inhibiting glioblastoma cell stemness [15]. [score:5]
These data confirm that miR-296 exerts a tumor suppressive role in CRC by inhibiting metastatic behaviors of CRC cells. [score:5]
showed that miR-296 overexpression in HT29 cells significantly increased the level of epithelial marker E-cadherin, and decreased the expression of mesenchymal markers including Vimentin and S100A4 (Fig.   4a). [score:5]
n = 3, * P < 0.05 Fig. 8S100A4 knockdown abrogates the effects of miR-296 inhibition on EMT, migration and invasion of CRC cells. [score:4]
These data indicate that S100A4 is a direct downstream target of miR-296. [score:4]
In azoxymethane (AOM) -treated rat mo del, miR-296-5p was downregulated in the uninvolved colonic mucosa (tumor field) of AOM rats [18]. [score:4]
Transfection of miR-296 mimic obviously up-regulated the level of miR-296 in HT29 cells (P < 0.05, Fig.   2a). [score:4]
Quantitative data indicated that miR-296 overexpression slightly reduced cell migration and invasion in S100A4 knockdown HT29 cells. [score:4]
miR-296 overexpression doesn’t notably reduced cell migration and invasion in S100A4 knockdown HT29 cells. [score:4]
c S100A4 knockdown significantly inhibited the migration and invasion of miR-296 silenced SW480 cells. [score:4]
miR-296 regulates S100A4 expression and epithelial-mesenchymal transition in CRC cells. [score:4]
In this study, miR-296 was found to be significantly downregulated in CRC tissues and cells. [score:4]
miR-296 post-transcriptionally regulates S100A4 expression. [score:4]
b S100A4 knockdown significantly inhibited the migration of miR-296 silenced SW480 cells. [score:4]
c Transwell assays confirmed that miR-296 overexpression inhibited HT29 cell migration and invasion. [score:4]
Lopez-Bertoni H, Lal B, Michelson N, Guerrero-Cazares H, Quinones-Hinojosa A, Li Y, Laterra J. Epigenetic modulation of a miR-296-5p: HMGA1 axis regulates Sox2 expression and glioblastoma stem cells. [score:4]
Furthermore, restoration of S100A4 expression could abrogate the anti-metastatic effects of miR-296 on HT29 cells with enhanced cell migration and invasion. [score:3]
In this study, we found that miR-296 could inhibit migration and invasion of CRC cells in vitro. [score:3]
Consequently, restoration of S100A4 promoted the metastatic behavior of miR-296 overexpressing HT29 cells with enhanced cell migration and invasion (P < 0.05, respectively, Fig.   7b and c). [score:3]
However, miR-296 expression contributed to the resistance to radiotherapy and tumor recurrence of laryngeal carcinoma [16], indicating an oncogenic role of miR-296 in laryngeal carcinoma. [score:3]
Fig. 1The status and prognostic value of miR-296 expression in CRC. [score:3]
Here, we confirmed that miR-296 was underexpressed in CRC specimens and cells. [score:3]
a miR-296 overexpressing HT29 cells that were infected with empty vector (EV) or S100A4 retroviruses were confirmed by western blotting for S100A4, E-cadherin and Vimentin. [score:3]
More importantly, decreased miR-296 was correlated with reduced overall survival and disease-free survival of CRC patients, and was found to be an independent factor for the prognosis of CRC patients. [score:3]
However, the expression and biological role of miR-296 in CRC remain unknown. [score:3]
Decreased expression of miR-296 has been found in metastatic colon cancer patients’ blood and AOM -induced CRC rat mo del [17, 18]. [score:3]
And decreased expression of miR-296 in CRC tissues conferred malignant clinical features of CRC patients including high tumor invasion stage, lymph node metastasis, distant metastasis, and advanced TNM stage. [score:3]
Our data disclosed that CRC tissues showed significant decreased expression levels of miR-296 (P < 0.05, Fig.   1a). [score:3]
A negative correlation between miR-296 and S100A4 expression was observed in CRC tissues. [score:3]
In representative immunohistochemical staining, miR-296 low expressing tumors showed strong staining of (a) S100A4 and (e) Vimentin, and weak staining of (c) E-cadherin. [score:3]
org) was used for discovery of the target molecule of miR-296. [score:3]
Underexpression of miR-296 correlates with adverse clinical parameters and poor prognosis of CRC patients. [score:3]
Furthermore, S100A4 is a downstream target of miR-296 in CRC. [score:3]
These data indicate that miR-296 can inhibit the metastasis of CRC cell by modulating EMT phenotype. [score:3]
Spearman’s correlation analysis indicated that miR-296 was strongly correlated with S100A4 (r = −0.784, P = 0.002), E-cadherin (r = 0.531, P = 0.013) and Vimentin (r = −0.638, P = 0.028) expression in CRC specimens. [score:3]
All together, our study demonstrates that miR-296 expression is significantly decreased in CRC. [score:3]
Study of lung cancer showed that miR-296 could inhibit the proliferation and enhanced the apoptosis of lung cancer cells [13, 14]. [score:3]
Scale bar: 50 μm We further explored whether S100A4 was a downstream target molecule of miR-296. [score:3]
n = 90. b The expression differences of miR-296 between 5 different CRC cells lines (HCT116, Caco2, HT29, SW620, SW480) and HIEC cells. [score:3]
miR-296 was found to play either oncogenic or tumor suppressive role in human cancers. [score:3]
miR-296 mimic, miR-296 inhibitor, S100A4 siRNA and the corresponding control vectors were bought from Genecopoeia (Guangzhou, China) and were then transduced into CRC cells with lippofectamine 2000 (Invitrogen, Carlsbad, CA, USA) following manufactures’ protocols. [score:3]
n = 3, * P < 0.05 Since we confirmed S100A4 was a target molecule of miR-296, S100A4 retroviruses were employed to disclose whether S100A4 restoration could abolish the anti-metastatic role of miR-296 in CRC cells. [score:3]
As shown in Table  1, CRC patients with low expression of miR-296 had high tumor invasion stage (P = 0.003), increased lymph node metastasis (P = 0.001) and distant metastasis (P = 0.025), and advanced tumor-node-metastasis (TNM) stage (P = 0.020). [score:3]
Our data showed that miR-296 inhibited the mobility and epithelial-mesenchymal transition (EMT) of cancer cells in CRC. [score:3]
n = 3, * P < 0.05. bs indicated that miR-296 overexpression reverses the migration of HT29 cells. [score:3]
n = 3, * P < 0.05 To disclose the underlying molecular mechanisms involved in the role of miR-296 in CRC cells, TargetScanHuman 7.1 (http://www. [score:3]
Underexpression of miR-296 was disclosed in CRC tissues and cells. [score:3]
Immunohistochemical staining of CRC specimens further confirmed the correlation between the expression of miR-296 and EMT markers. [score:3]
Taken together, these experiments suggest that S100A4 is not only a downstream target but also a mediator of miR-296 in CRC. [score:3]
Moreover, we disclosed that S100A4 was the major functional target of miR-296 in CRC. [score:3]
miR-296 expression is decreased in CRC. [score:3]
Furthermore, survival analyses indicated that patients with low expression of miR-296 showed significantly reduced 5-year overall and recurrence-free survival (P = 0.046 and P = 0.006, respectively, Fig.   1c and d). [score:3]
Accordingly, the levels of miR-296 were obviously down-regulated in CRC cells compared to HIEC cells. [score:3]
b S100A4 restoration significantly promoted the migration of miR-296 overexpressing HT29 cells. [score:3]
These data indicate miR-296 probably plays a suppressive role in CRC. [score:3]
miR-296 inhibits the mobility of CRC cells. [score:3]
The expression of miR-296 was confirmed by qRT-PCR in CRC tissues and cells, and its level was altered by corresponding miRNA vectors. [score:3]
miR-296 low expressing tumors showed strong staining of S100A4 (Fig.   5a) and Vimentin (Fig.   5e), and weak staining of E-cadherin (Fig.   5c). [score:3]
Mechanically, miR-296 exerted an anti-metastatic function by suppressing EMT and S100A4 abundance in CRC cells. [score:3]
However, miR-296 high expressing tumors showed weak staining of (b) S100A4 and (f) Vimentin, and strong staining of (d) E-cadherin. [score:3]
And miR-296 inhibits the EMT and metastasis of CRC cells. [score:3]
Altogether, miR-296 potentially act as a prognostic predictor and a drug-target for CRC patients. [score:3]
miR-296 functions as an anti-metastatic factor mainly by suppressing S100A4 in CRC. [score:3]
a The expression differences of miR-296 between CRC tissues and normal tumor-adjacent tissues. [score:3]
Then, the wt 3’-UTR of S100A4 or mt 3’-UTR of S100A4, and miR-296 mimic or miR-296 inhibitor were co-transduced into CRC cells by lippofectamine 2000 (Invitrogen). [score:3]
c S100A4 restoration evidently facilitated cell migration and invasion in miR-296 overexpressing HT29 cells. [score:3]
Mechanically, miR-296 inhibited the epithelial-mesenchymal transition (EMT) of CRC cells. [score:3]
In turn, miR-296 inhibitor significantly decreased the level of miR-296 in SW480 cells (P < 0.05, Fig.   3a). [score:3]
Therefore, miR-296 plays a tumor suppressive role in CRC and could potentially serve as a promising biological tag for the prognosis of patients. [score:3]
These suggest that S100A4 is not only a downstream target but also a mediator of miR-296 in CRC. [score:3]
In vitro experiments indicated that miR-296 inhibited CRC cell migration and invasion. [score:3]
However, miR-296 high expressing tumors showed weak staining of S100A4 (Fig.   5b) and Vimentin (Fig.   5f), and strong staining of E-cadherin (Fig.   5f). [score:3]
s indicated that miR-296 inversely regulated the luciferase activity of 3’-UTR of S100A4. [score:2]
n = 3, * P < 0.05. b miR-296 knockdown notably facilitated the migration of SW480 cells. [score:2]
The wound healing assays showed that miR-296 overexpression notably reduced cell migration in HT29 cells (Fig.   2b). [score:2]
And Transwell assays explored that ectopic expression of miR-296 significantly reduced the numbers of migrated and invaded HT29 cells (P < 0.05, respectively, Fig.   2c). [score:2]
c miR-296 knockdown prominently promoted SW480 cell migration and invasion. [score:2]
Next, we compared the expression levels of miR-296 between CRC cells lines and HIEC cells. [score:2]
In turn, S100A4 knockdown abolished the effects of miR-296 silencing on EMT, migration and invasion of SW480 cells (P < 0.05, respectively, Fig.   8a-c). [score:2]
Moreover, S100A4 was identified as a downstream molecule of miR-296 and mediated the biological functions of miR-296 in CRC. [score:1]
U6 was used as the control gene for the relative level of miR-296. [score:1]
Thus, miR-296 exerts a anti-metastatic role in CRC cells. [score:1]
To examine the status of miR-296 in CRC, qRT-PCR was performed on 90 CRC cases. [score:1]
A significant correlation between miR-296 and S100A4, E-cadherin and Vimentin was confirmed in CRC specimens. [score:1]
Recently, miRNA-296 was found to play important roles in various human cancers including lung cancer [13, 14], glioblastoma [15], bladder cancer [16], and laryngeal carcinoma [16]. [score:1]
Previous study has reported that decrease in blood miR-296 predicts chemotherapy resistance and poor clinical outcome in patients receiving systemic chemotherapy for metastatic colon cancer [17]. [score:1]
S100A4 mediates the anti-metastatic effects of miR-296 on CRC cells. [score:1]
a HT29 cells that were transduced with negative control mimics (miR-control) or miR-296 mimics were confirmed by qRT-PCR. [score:1]
a miR-296 silenced SW480 cells that were transfected with S100A4 siRNA and scrambled siRNA (scr siRNA) were subjected to western blot. [score:1]
And alteration of miR-296 did not have any influence on the luciferase activity of mt 3’-UTR of S100A4 (Fig.   6b). [score:1]
Herein, S100A4 was found to be a downstream molecule of miR-296 in CRC. [score:1]
Subsequently, miR-296 silencing notably facilitated SW480 cell migration and invasion (P < 0.05, respectively, Fig.   3b and c). [score:1]
Alteration of miR-296 had no effect on the luciferase activity of mt 3’-UTR of S100A4. [score:1]
The low level of miR-296 correlated with adverse clinical features of CRC patients and decreased survival rate. [score:1]
miR-296 Colorectal cancer Metastasis Epithelial-mesenchymal transition S100A4 Colorectal cancer (CRC), which is the third most common cancer worldwide, is the fourth most common cause of cancer-related deaths [1]. [score:1]
a The binding sites for miR-296 in wild type (wt) and mutant (mt) 3’-UTR of S100A4. [score:1]
miR-296 was previously found to be a cancer-related miRNAs. [score:1]
n = 3, * P < 0.05 To examine the status of miR-296 in CRC, qRT-PCR was performed on 90 CRC cases. [score:1]
Moreover, we found that miR-296 could directly interact with the 3’-UTR of S100A4 using luciferase reporter assay. [score:1]
Recent study reported that decreased in blood miR-296 predicted chemotherapy resistance and poor clinical outcome in patients receiving systemic chemotherapy for metastatic colon cancer. [score:1]
Yet, the clinical value and biological function of miR-296 remain rarely known in CRC. [score:1]
S100A4 knockdown HT29 cells that were transfected with negative control mimics (miR-control) and miR-296 mimics, respectively, were subjected to Transwell assays for cell migration and invasion. [score:1]
However, the status of miR-296 and its function in CRC remain unknown. [score:1]
As shown in Fig.   6a, the putative bind sites for miR-296 was presented in the 3’-UTR of S100A4. [score:1]
Fig. 7S100A4 restoration reverses the effects of miR-296. [score:1]
These indicate that miR-296 plays different roles in different cancer types. [score:1]
Furthermore, S100A4 mediated the anti-metastatic effects of miR-296 on EMT, migration and invasion of CRC cells. [score:1]
We suggest that miR-296 is a possible prognostic biomarker for CRC patients. [score:1]
The low level of miR-296 correlates with adverse clinical parameters of CRC patients and shortened survival. [score:1]
[*] Statistically significant Since increased cancer cell mobility is a important reason for the metastasis and recurrence of human cancer [20], we explored whether miR-296 could modulate the migration and invasion of CRC cells. [score:1]
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[+] score: 172
We identified 1 validated target of miR-296-3p; 5 validated targets of miR-298-5p; 207 predicted targets of miR-296-3p; 707 predicted targets of miR-298-5p. [score:9]
Four of them (HMX2, HNF4A, LEF1, MAFB) are known to be expressed in the islets of Langerhans, and MAFB is known to be expressed only in rodent islet α cells within adult pancreas [25]; the presence of binding sites for this TF within the promoter of the genes encoding miR-296-3p and miR-298-5p suggests that it may regulate the expression of both miRNAs. [score:8]
Altogether, high-throughput microRNA profiling, functional analysis with synthetic mimics and molecular characterization of modulated pathways strongly suggest that specific downregulation of miR-296-3p and miR-298-5p, coupled to upregulation of their targets as IGF1Rβ and TNFα, is a major determinant of mammalian pancreatic α cells resistance to apoptosis induction by cytokines. [score:7]
HT miRNA profiling data, functional analysis with synthetic mimics and molecular characterisation of modulated pathways strongly suggest that specific downregulation of miR-296-3p and miR-298-5p in pancreatic α cells, coupled to upregulation of their targets as IGF1Rβ and TNFα and activation of the corresponding signaling pathways, is a major determinant of their resistance to apoptosis induction by cytokines. [score:7]
Within the network of genes regulated by α-miRNAs, insulin-like growth factor receptor signaling pathway is a biological process significantly enriched among the genes interacting with targets of miR-296-3p and miR-298-5p, with respect to the genes linked to the targets of the other miRNAs (p-value = 0.039, Fisher’s exact test). [score:6]
Among them, Bcl2, Ccna2, Irs2, Nr4a2 are transcriptionally regulated by CREB1, which is a validated target of miR-296-3p [22]; Tnf and Vdr are validated targets of miR-298-5p [23, 24]. [score:6]
We focused our study on two microRNAs, miR-296-3p and miR-298-5p, which were: (1) specifically expressed at steady state in αTC1-6, but not in βTC1 or INS-1 cells; (2) significantly downregulated in αTC1-6 cells after treatment with cytokines in comparison to untreated controls. [score:6]
Modulation of miR-296-3p and miR-298-5p also alters expression of their targets. [score:5]
To verify whether in vitro modulation of miR-296-3p and miR-298-5p affected the expression of their targets, we performed transient transfection experiments of αTC1-6 cells with their mimics. [score:5]
Our computational analysis suggests that MAFB (a transcription factor exclusively expressed in pancreatic α cells within adult rodent islets of Langerhans) controls the expression of miR-296-3p and miR-298-5p. [score:5]
Figure 4 Modulation of miR-296-3p and miR-298-5p alters expression of their targets. [score:5]
Although its biological effect was potentiated when also miR-296-3p was expressed, our results suggest that the role of miR-298-5p is more important in this process than that of miR-296-3p (Figure  3): this would highlight the role of one or a few specific miR-298-5p targets. [score:5]
Bar graph showing changes in gene expression of a selected set of miR-296-3p and miR-298-5p targets for each of three different experimental conditions: (i) αTC1-6 treated with cytokines with respect to matched untreated control cells at the time points 24 and 48 h; (ii) untreated αTC1-6 transfected with mimics of miR-296-3p with respect to scramble -transfected control cells at the time points 24 and 48 h; (iii) untreated αTC1-6 transfected with mimics of miR-298-5p with respect to scramble -transfected control cells at the time points 24 and 48 h. Data are reported as LOG of 2^ [-ΔΔCt] values. [score:5]
Single TaqMan gene expression assays (STAs) during a time course analysis (6-12-24-48 h) showed a highly significant downregulation of miR-296-3p in αTC1-6 cells at 24 and 48 h PT, compared to matched untreated controls (Student’s t-test, Bonferroni adjusted p-value < 0.01). [score:4]
By exploiting specific microRNA mimics, we demonstrated that experimental upregulation of miR-296-3p and miR-298-5p raised the propensity to apoptosis of transfected and cytokine -treated αTC1-6 cells with respect to αTC1-6 cells, treated with cytokines after transfection with scramble molecules. [score:4]
Figure 3 Upregulation of miR-296-3p and miR-298-5p reduces αTC1-6 resistance to apoptosis induced by cytokines. [score:4]
Figure 5 Expression of IGF1Rβ and TNFα proteins is regulated by miR-296-3p and miR-298-5p in αTC1-6. (A) of IGF1Rβ in (1) untreated αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p (left); (2) αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p and treated with cytokines for further 24 h (middle); (3) αTC1-6 treated with cytokines for 24 h and their matched untreated controls (right). [score:4]
Expression of IGF1Rβ and TNFα is controlled by miR-296-3p and miR-298-5p in αTC1-6 cells. [score:3]
Decreased expression of mir-296-3p and miR-298-5p and the corresponding activation of survival and proliferation signals, mediated by IGF1R and its downstream nodes (e. g., IRS-1 and ERK-1), may thus explain why αTC1-6 cells are resistant to death induction by cytokines (see Additional file 13). [score:3]
Through western analysis, we confirmed our computational prediction that IGF1Rβ and TNFα are common targets to both miRNAs and that miR-296-3p and miR-298-5p also control IRS-1 and ERK-1 within the IGF1R signaling pathway. [score:3]
The expression of phospho-IRS-1 didn’t change in untreated αTC1-6 transfected with mimics of each miRNA alone, while it decreased about 1.5 folds in αTC1-6 transfected with mimics of both miR-296-3p and miR-298-5p (Figure  6A, left panel). [score:3]
Figure 2 Expression of miR-296-3p and miR-298-5p in αTC1-6 and βTC1. [score:3]
Validated and predicted targets of miR-296-3p and miR-298-5p. [score:3]
We focused our attention on 7 targets of miR-296-3p, 4 of miR-298-5p, 2 common to both miRNAs: they were chosen according to their involvement in apoptosis, cell cycle progression, cell differentiation and hormone secretion (see Additional file 8). [score:3]
Scatter plot showing correlation between miR-296-3p (x-axis) and miR-298-5p (y-axis) expression in αTC1-6, during a 6-12-24-48 h time-course experiment. [score:3]
Identification of miR-296-3p and miR-298-5p targets. [score:3]
In αTC1 transfected with mimics of miR-296-3p or miR-298-5p, real-time PCR showed altered expression of different genes with respect to scramble -transfected cells, including Igf1r, Tnf, Vdr (Figure  4). [score:3]
Click here for file Validated and predicted targets of miR-296-3p and miR-298-5p. [score:3]
A selection of validated and predicted targets of miR-296-3p and miR-298-5p was chosen according to their involvement in apoptosis, cell cycle progression, cell differentiation and hormone secretion. [score:3]
Click here for file Scatter plot showing correlation between miR-296-3p (x-axis) and miR-298-5p (y-axis) expression in αTC1-6, during a 6-12-24-48 h time-course experiment. [score:3]
Following transfection of αTC1-6 with either mimics of miR-296-3p or miR-298-5p, TNFα protein was about 1.2 folds less expressed with respect to scramble -transfected controls; this decrease was more pronounced (1.6 folds) when cells were transfected with both mimics (Figure  5B, left panel). [score:3]
Expression of a macro-noncoding RNA (precursor of miR-296, miR-298, Nespas) is predicted to be controlled by two groups of CpG islands (one comprising two CpG islands, from 17.5 to 18.8 kb upstream the first nucleotide of pre-miR-296; the other made of three CpG islands, from 30.1 to 33.6 Kb upstream the first nucleotide of pre-miR-296). [score:3]
Interestingly, also the activation of ERK-1 appears to be regulated by miR-296-3p and miR-298-5p: in the absence of treatment with cytokines, αTC1-6 cells transfected with mimics of miR-296-3p showed levels of phospho-ERK-1 (Thr202) similar to those found in scramble -transfected αTC1-6 cells; the transfection with mimics of miR-298-5p or of both miRNAs led instead to a decrease of the protein (1.2 and 1.3 folds, respectively) (Figure  6B, left panel). [score:2]
Hypothetical mo del of regulation of miR-296-3p and miR-298-5p biomolecular activity in αTC1-6 at steady state (left) and after treatment with cytokines (right). [score:2]
Phospho-IRS1 (Tyr612) and Phospho-ERK-1 (Thr202), which we demonstrated to be controlled by miR-296-3p and miR-298-5p, are known to regulate the response to insulin and to be involved in survival and proliferation processes [30]. [score:2]
Click here for file 3 Hypothetical mo del of regulation of miR-296-3p and miR-298-5p biomolecular activity in αTC1-6 at steady state (left) and after treatment with cytokines (right). [score:2]
Transient transfection of αTC1-6 cells with mimics of miR-296-3p and miR-298-5p. [score:1]
αTC1-6 transfection with mimics of miR-296-3p and miR-298-5p increases apoptosis levels induced by cytokines. [score:1]
By using the same controls, we detected a slight decrease of phospho-IRS-1 (1.2 folds) in αTC1-6 transfected with mimics of both miR-296-3p and miR-298-5p and treated with cytokines (Figure  6A, right panel). [score:1]
On scale representation of the genome segment comprising Nespas, miR-296, miR-298. [score:1]
At 24 h PT, αTC1-6 transfected with mimics of miR-298-5p show a highly significant increase of the number of apoptotic cells with respect to scramble -transfected control; at the same time point, in αTC1-6 transfected with mimics of both miR-296-3p and miR-298-5p a highly significant increase of the number of apoptotic cells is detected with respect to all the other experimental conditions. [score:1]
Transfections were performed using siPORT™ NeoFX™ (Lifetechnologies™) with 30 nM mimics of miR-296-3p/miR-298-5p/scrambled sequence (Pre-miR™ miRNA Precursor Molecules—Negative Control #1, Lifetechnologies™). [score:1]
Figure 6 Activation of IRS-1 and ERK-1 is under control of miR-296-3p and miR-298-5p in αTC1-6. (A) of phospho-IRS-1 (Tyr612) in (1) untreated αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p (left); (2) αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p and treated with cytokines for further 24 h (right). [score:1]
Genomics of genes encoding miR-296-3p, miR-298-5p, Nespas and identification of upstream CpG islands. [score:1]
Among them, miR-296-3p and miR-298-5p stood out clearly as potentially critical nodes, responsible for α cells resistance to cytokine -induced cell death. [score:1]
Sequences of mature miR-296-3p are 100% conserved between rodents and humans, whereas those of miR-298-5p are 74% identical. [score:1]
CpG islands upstream genes encoding miR-296, miR-298, Nespas were identified through UCSC Genome Browser (http://genome. [score:1]
Our results suggest that miR-296-3p and miR-298-5p play a pivotal role in determining this trait. [score:1]
The decrease of IGF1Rβ was not detectable in αTC1-6 transfected with either mimic of miR-296-3p or miR-298-5p and then treated with cytokines for 24 h. In αTC1-6 treated with cytokines for 24 h, after transfection with mimics of both miRNAs 296-3p and 298-5p, it was instead lower than at steady state (1.4 folds). [score:1]
In the genomic region comprising the genes encoding miR-296-3p, miR-298-5p and Nespas, MatInspector identified Transcription Factor Binding Sites (TFBS) for sixty seven Transcription Factors (TFs). [score:1]
Activation of IRS-1 and ERK-1 is also under control of miR-296-3p and miR-298-5p. [score:1]
Finally, χ [2]-square test was used to establish if miR-296-3p and miR-298-5p have more common targets than expected by chance; Fisher’s exact test was applied to evaluate the enrichment in specific gene ontologies. [score:1]
Analysis of this region through UCSC browser revealed the presence of two clusters of CpG islands: (i) one comprises two CpG islands, from 17.5 to 18.8 kb upstream the first nucleotide of pre-miR-296, and is located 9.2 and 10 Kb downstream Nespas transcription start site (TSS); (ii) the other is made of three CpG islands from 30.1 to 33.6 Kb upstream the first nucleotide of pre-miR-296 and is located 1.8-5 kb upstream Nespas TSS (see Additional file 7). [score:1]
For each time point DCt values of miR-296-3p and miR-298-5p were correlated, both from untreated and cytokines -treated αTC1-6 cells (r-value = 0.88, p-value = 1.15e-08, Pearson’s correlation test). [score:1]
Genomics of genes encoding miR-296-3p, miR-298-5p, Nespas and identification of upstream CpG islandsGenes encoding miRNAs 296-3p and 298-5p are clustered in a genomic region, which also comprises the gene for the noncoding transcript Nespas and is imprinted in mice and humans [21]. [score:1]
For analysis of correlation between the expression of miR-296-3p and miR-298-5p in αTC1-6, Pearson correlation coefficient was calculated. [score:1]
The percentage of apoptotic αTC1-6 cells after transfection with mimics of miR-296-3p was comparable to scramble -transfected controls during the entire time course treatment. [score:1]
Click here for file On scale representation of the genome segment comprising Nespas, miR-296, miR-298. [score:1]
org predicts two binding sites for mmu-miR-296-3p and mmu-miR-298-5p on Mafb mRNA 3’ UTR. [score:1]
Their assignment to specific families is shown in Additional file 5. To identify miRNAs whose functions could explain the differential response to cytokines of pancreatic α and β cells, we specifically focused our attention on miR-296-3p and miR-298-5p. [score:1]
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0012362.g004 Figure 4Analysis of the miR-296 predicted target gene TSC2 and 11 let-7 predicted target genes in vitro. [score:5]
To study whether TSC2 is the target of miR-296, we prepared a TSC2 3′UTR reporter construct and examined the luciferase activity by treated cells with control, miR-296 mimic and inhibitor. [score:5]
Analysis of the miR-296 predicted target gene TSC2 and 11 let-7 predicted target genes in vitro. [score:5]
The findings indicated that TSC2 was not a direct target of miR-296. [score:4]
A Transient transfection analysis for luciferase reporter expression with TSC2 3′UTR in the presence and absence of miR-296. [score:3]
B Immunoblotting analysis of transient transfection analysis of miR-296 for TSC2 expression. [score:3]
Mature microRNAs mimics and inhibitors from let-7c and miR-296 were purchased from Dharmacon Inc. [score:3]
There was no reduction of luciferase expression in cell treated with miR-296 (Figure 4A). [score:3]
We further examined whether miR-296 could inhibit TSC2 protein production. [score:3]
The inverse correlation of TSC and miR-296 levels may thus be related to indirect or unrelated molecular mechanisms participating in ULM tumorigenesis. [score:2]
By correlation analysis, as illustrated in Figure 2, we found that predicted regulatory miR-296 was inversely correlated with TSC2 protein in 36 ULMs. [score:2]
In comparison to TSC2 siRNA, no significant protein reduction was noted in cells treated with miR-296 (Figure 4B). [score:1]
However, in the TSC2 3′UTR immediately adjacent to the stop codon, there is a highly conserved sequence that harbors the complementary sites of miR-296 and a few other microRNAs. [score:1]
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5
[+] score: 38
After normalization to 1 in the control group (U937/GFP), the relative expressions of selected downregulated miRNAs (miR-27a-3p, miR-424-5p, and miR-496-5p) in the test group are shown in A; the relative expressions of upregulated miRNAs (miR-296-5p, miR-377-5p, and miR-3680-5p), and unchanged miR-191-5p in the test group are shown in B. Figure 3 qPCR validation of miRNA expression levels in samples from the latent tuberculosis infection (LTBI) group versus the healthy control group. [score:13]
After normalization to 1 in the control group (U937/GFP), the relative expressions of selected downregulated miRNAs (miR-27a-3p, miR-424-5p, and miR-496-5p) in the test group are shown in A; the relative expressions of upregulated miRNAs (miR-296-5p, miR-377-5p, and miR-3680-5p), and unchanged miR-191-5p in the test group are shown in B. Figure 3 qPCR validation of miRNA expression levels in samples from the latent tuberculosis infection (LTBI) group versus the healthy control group. [score:13]
In parallel, the levels of upregulated miR-296-5p, miR-377-5p, miR-3680-5p, and unchanged miR-191-5p were similar to the chip results as well (Figure 2B). [score:4]
As shown in Figure 3, the results of four miRNAs (miR-424-5p, miR-27a-3p, miR-377-5p, miR-3680-5p) recapitulated the microarray data, and the other two miRNAs (miR-493-5p and miR-296-5p) were not significant differentially expressed. [score:3]
The expression level of seven miRNAs (miR-424-5p, miR-493-5p, miR-296-5p, miR-27b-3p, miR-377-5p, miR-3680-5p, miR-191-5p) were validated by qRT-PCR. [score:3]
000631hsa-miR-296-5p2.710.0495120hsa-miR-4685-3p5.040.0009010hsa-miR-150-5p2.850.0092719hsa-miR-23c5.110.00081Xhsa-miR-45402.860.012809hsa-miR-5002-3p5.140.000353hsa-miR-42682.970.009692hsa-miR-56895.330.000546hsa-miR-12363.080.048776hsa-miR-9355.430.0018719hsa-miR-221-5p3.160.03132Xhsa-miR-374b-3p5.795.4E-05Xhsa-miR-36853.260.0035612hsa-miR-1255b-2-3p5.830.008231hsa-let-7d-3p3.350.021539hsa-miR-485-3p6.000. [score:1]
The miR-424-5p (previous ID: miR-424), miR-493-5p (previous ID: miR-493*), and miR-296-5p were reported as potential to discriminate between latent TB and healthy by the previous study [12], the other four miRNAs (miR-27b-3p, miR-377-5p, miR-3680-5p, miR-191-5p) were randomly selected. [score:1]
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[+] score: 36
Regarding these observations, we performed qRT-PCR for 8 target genes of commonly regulated miRNA; 4 target genes (ATG5, ITGA6, NCKAP1, SARBS1) of the 2 up-regulated miRNA (mmu-miR-291b-5p, mmu-miR-296-5p) and 4 target genes (AKT1, APC, LMO7, MSN) of the 3 down-regulated miRNA (mmu-miR-30c-1*, mmu-miR-467b* and mmu-miR-374*). [score:14]
Interestingly, in cluster A, 3 miRNAs (mmu-miR-30c-1*, mmu-miR-374* and mmu-miR-497b*) were identified as being down-regulated by all nine polyphenols tested, while in cluster 2, 2 miRNAs (mmu-miR-291b-5p and mmu-miR-296-5p) were observed as up-regulated by all nine polyphenols (Table 2). [score:7]
Regarding miR-296-5p, its expression has been observed to be down-regulated in endothelial cells exposed to inflammatory stimulus [30]. [score:6]
Different studies have been reported regarding miR-296 for which the expression has been observed to be down-regulated in the mouse brain after prenatal ethanol exposure and has been shown to be associated with mental retardation [31], or parathyroid cancer tissue [32] or even NIH3T3 cells exposed to UV irradiation that induces apoptosis and necrosis. [score:6]
Moreover, changes in miRNA expression were observed after polyphenol supplementation, and five miRNAs (mmu-miR-291b-5p, mmu-miR-296-5p, mmu-miR-30c-1*, mmu-miR-467b* and mmu-miR-374*) were identified as being commonly modulated by these polyphenols. [score:3]
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[+] score: 33
A high expression of hsa-miR-296-5p may result in suppression of BCL2 transcription which, in turn, could lead to higher rates of cell death. [score:5]
The expression of hsa-miR-103a-3p, hsa-miR-211, hsa-miR-296-5p, hsa-miR-1233 and hsa-miR-1267 in whole saliva and the absence of these miRNAs in parotid saliva suggest that these miRNAs are not specifically expressed and/or secreted from the parotid gland tumor. [score:5]
One of the validated targets for hsa-miR-296-5p is the B-cell lymphoma 2 gene, (BCL2) a member of the Bcl2 -family of apoptosis regulator proteins. [score:4]
Of these, 5 miRNAs (hsa-miR-296-5p, hsa-miR-577, hsa-miR-1233, hsa-miR-1267, and hsa-miR-1825) had a significantly higher expression level (lower ΔCt) in whole saliva samples from patients with a parotid gland neoplasm compared to their expression levels in whole saliva from healthy controls. [score:4]
Four of the five tumor-specific miRNAs (hsa-miR-296-5p, hsa-miR-1233, hsa-miR-1267, and hsa-miR-1825) had a significantly higher expression level in whole saliva from patients than in whole saliva from healthy controls (Table 3). [score:3]
The targets for hsa-miR-211, hsa-miR-296-5p and hsa-miR-425-5p have only been validated in tissue and not in saliva itself. [score:3]
Three of the discovered miRNAs (hsa-miR-211, hsa-miR-296-5p, and hsa-miR-425-5p) had validated targets. [score:3]
Therefore, we can only speculate what role hsa-miR-211, hsa-miR-296-5p and hsa-miR-425-5p play in saliva. [score:1]
miRNA ΔCt control mean (sd) ΔCt neoplasm mean (sd) Wilcoxon 2-sided p-value hsa-miR-103a-3p 6.34 (1.71) ND < 0.001 hsa-miR-211 9.45 (1.38) ND < 0.001 hsa-miR-425-5p 11.56 (3.72) ND < 0.001 hsa-miR-296-5p ND 7.41 (3.75) < 0.001 hsa-miR-577 ND 5.96 (3.44) < 0.001 hsa-miR-1233 19.14 (4.98) 8.93 (8.49) 0.002 hsa-miR-1267 ND 3.87 (2.79) < 0.001 hsa-miR-1825 20.94 (2.26) 5.17 (5.38) < 0.001 ND: non-detectable, assigned to samples with a Ct-value of 40 and higher. [score:1]
The full mo del with 7 miRNA markers (hsa-miR-103a-3p, hsa-miR-211, hsa-miR-296-5p, hsa-miR-425-5p, hsa-miR-1233, hsa-miR-1267 and hsa-miR-1825) yielded an AUC of 0.95 (95% CI: 0.88–1.00), a sensitivity of 93% and a specificity of 86%. [score:1]
miRNA ΔCt control mean(sd) ΔCt neoplasm mean (sd) Wilcoxon 2-sided p-value hsa-miR-103a-3p 14.32 (3.59) 10.00 (4.75) < 0.001 hsa-miR-211 14.91 (3.18) 8.56 (4.37) < 0.001 hsa-miR-296-5p 12.80 (4.15) 6.95 (4.66) < 0.001 hsa-miR-425-5p 9.96 (5.13) 2.54 (4.79) < 0.001 hsa-miR-577 10.19 (1.57) 9.66 (2.85) 0.650 hsa-miR-1233 15.74 (0.70) 9.17 (6.89) < 0.001 hsa-miR-1267 9.78 (5. 03) 4.39 (5.21) < 0.001 hsa-miR-1825 7.47 (7.46) -0.77 (3.95) < 0.001 Multivariate logistic regression mo dels with these miRNA biomarkers were constructed for the classification of patient samples into parotid gland neoplasm and healthy categories. [score:1]
miRNA ΔCt control mean(sd) ΔCt neoplasm mean (sd) Wilcoxon 2-sided p-value hsa-miR-103a-3p 14.32 (3.59) 10.00 (4.75) < 0.001 hsa-miR-211 14.91 (3.18) 8.56 (4.37) < 0.001 hsa-miR-296-5p 12.80 (4.15) 6.95 (4.66) < 0.001 hsa-miR-425-5p 9.96 (5.13) 2.54 (4.79) < 0.001 hsa-miR-577 10.19 (1.57) 9.66 (2.85) 0.650 hsa-miR-1233 15.74 (0.70) 9.17 (6.89) < 0.001 hsa-miR-1267 9.78 (5. 03) 4.39 (5.21) < 0.001 hsa-miR-1825 7.47 (7.46) -0.77 (3.95) < 0.001 Samples were collected from patients with a parotid gland neoplasm (n = 46) and controls (n = 14). [score:1]
The full mo del included 7 miRNAs (hsa-miR-103a-3p, hsa-miR-211, hsa-miR-296-5p, hsa-miR-425-5p, hsa-miR-1233, hsa-miR-1267 and hsa-miR-1825). [score:1]
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[+] score: 25
Other miRNAs from this paper: hsa-let-7b, hsa-mir-21, hsa-mir-27a, hsa-mir-148a, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-141, hsa-mir-126, hsa-mir-146a, hsa-mir-1-1, hsa-mir-155, hsa-mir-34b, hsa-mir-34c, hsa-mir-370, hsa-mir-373, hsa-mir-342, hsa-mir-526a-1, hsa-mir-526a-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-542, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1246, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-548q, hsa-mir-548s, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-203b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
MiR-296-5p is upregulated, while miR-23b is downregulated in EV71 infection. [score:7]
Meanwhile, the suppression of endogenous miR-296-5p promoted EV71 replication, and the introduction of mutations into binding sites on the viral genome led EV71 to escape the inhibitory effects of miR-296-5p [56]. [score:6]
EV71 infection -induced miR-296-5p could target both viral VP1 and VP3 regions and result in the inhibition of virus replication. [score:5]
Zheng Z. Ke X. Wang M. He S. Li Q. Zheng C. Zhang Z. Liu Y. Wang H. Human microRNA hsa-miR-296-5p suppresses enterovirus 71 replication by targeting the viral genome J. Virol. [score:5]
The induction of miRNA-296-5p was found in EV71-infected human rhabdomyosarcoma (RD) and SK-N-SH cells, and the silicon analysis results predicted that miRNA-296-5p might target both the VP1 and VP3 regions of the viral genome; this speculation was confirmed by molecular biological assays (Figure 2) [56]. [score:2]
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[+] score: 24
The enterovirus EV71 infection induces the expression of miR-296-5p, which targets the coding region of the viral RNA and inhibits viral replication [211]; interestingly, the virus acquired mutations that enabled it to evade miR-296-5p -mediated suppression. [score:10]
The human IFNβ was reported to induce the expression of cellular miRNAs miR-196, miR-296, miR-351, miR-431, and miR-448, which displayed seed-sequence complementarity with HCV RNA genome and downregulated virus replication; conversely, the IFNβ was shown to downregulate the HCV cofactor miR-122, thereby causing a reduction in HCV replication [209]. [score:9]
Zheng Z. Ke X. Wang M. He S. Li Q. Zheng C. Zhang Z. Liu Y. Wang H. Human microRNA hsa-miR-296-5p suppresses enterovirus 71 replication by targeting the viral genomeJ. [score:5]
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[+] score: 21
The expression of mir-296-5p (p = 0.002), mir-122 (p<0.001), mir-448 (p<0.001) and mir-128 (p<0.001) was significantly down-regulated in patients with chronic hepatitis C compared to normal non-infected patients (Fig. 2C). [score:5]
None of the miRNAs regulating HCV replication in vitro (mir-196b p = 0.499, mir-296-5p p = 0.253, mir-431 p = 0.128, mir-448 p = 0.971) showed difference of expression prior to treatment, in NRs and SVRs (Fig. 2C). [score:4]
Moreover, IFNα/β up-regulates several cellular miRNAs (mir-196, mir-296, mir-351, mir-431, mir-1, mir-30 and mir-128 and mir-448) with putative recognition sites within HCV genome [17]. [score:4]
The aim was to study the expression of 6 miRNAs (mir-122, mir-196b, mir-296-5p, mir-448, mir-431 and mir-218) and 30 mRNAs (S1 Table). [score:3]
2C- The expression of mir-122, mir-196b, mir-296-5p, mir-448, mir-431 and mir-128 was analyzed by RT q-PCR in the total group of patients (n = 111). [score:3]
Mir-196, mir-296, mir-351, mir-431 and mir-448 were indeed able to substantially attenuate viral replication [17]. [score:1]
MiR-196, miR-296-5p, miR-431 and miR-448 are all induced by IFN α/β and contain putative recognition sites within HCV genome [17]. [score:1]
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[+] score: 21
Several examples are: miR-17-92 which is upregulated in colonocytes coexpressing K-Ras and c-Myc, represses the expression of anti-angiogenic thrombospondin-1 (Tsp1) and connective tissue growth factor (CTGF), thus induces angiogenesis [17]; miR-378 promotes angiogenesis induced by human glioblastoma cell line U87 by targeting Fus-1 expression [18]; miR-126 regulates vascular integrity and angiogenesis, and miR-126 restoration decreases VEGF level in lung cancer cells [19], [20]; miR-130a mediates angiogenesis through downregulating antiangiogenic homeobox genes GAX and HOXA5 [21]; miR-296 level is elevated in primary brain tumor endothelial cells and regulates angiogenesis by directly targeting the hepatocyte growth factor-regulated tyrosine kinase substrate mRNA, leading to the reduction of HGS -mediated degradation of the growth factor receptors VEGFR2 and PDGFRbeta [22]. [score:21]
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[+] score: 20
E2f1, which was significantly up-regulated after treatment with 0.1 mg/kg bw furan, was the predicted target of down- regulated rno-miR-296. [score:7]
In the present study, rno-miR-296 showed the greatest change in expression (~ 8-fold down-regulation). [score:6]
Human miR-296 has been reported to be down-regulated in breast cancer and parathyroid cancer (Barh et al. 2008; Corbetta et al. 2010). [score:4]
Furthermore, inhibition of miR-296 in Hela cells has been reported to decrease cell growth and increase the level of apoptosis (Cheng et al. 2005). [score:3]
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[+] score: 19
Several of these IFN -induced miRNAs (miR-1, miR-30, miR-128, miR-196, miR-296) are expressed in peripheral blood mononuclear cells (PBMCs) from healthy individuals and from chronic HCV-infected patients, and their expression is upregulated by IFN treatment to varying degrees [22]. [score:8]
We found that while expression of F705-STAT3 also blocked the IFN induction of miR-351 and miR-296, it had no effect on IFN -induced miR-196a expression. [score:5]
In addition, since miR-196a, miR-296 and miR-351 were found to be IFN -induced miRNAs [16], we explored the role of STAT3 in their IFN -induced expression. [score:3]
Therefore, these results indicate that the expression of a subset of IFN-inducible miRNAs (miR-21, miR-351 and miR-296) is highly dependent on STAT3 activation. [score:3]
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[+] score: 15
To correct (to the extent possible) for this difference, we excluded a further 20 target sites with GU pairs and mismatches in the seed region for miR-134, and 8 target sites for miR-296 (all target sites for miR-375 have WC matches in the seed region), and report the results of 65 target genes examined for miR-134, 6 for miR-296 (for miR-296, all six sites examined were validated), and 22 for miR-375. [score:9]
miRNA Condition Number of targets miR-134 WC bp at nt 2–7 True positives 43 Sensitivity = 0.551 False negatives 35 Specificity = 0.666 False positives 3 True negatives 6 Total 87 WC bp at nt 2–7, and 40% FE threshold (−18.64) True positives 36 Sensitivity = 0.462 False negatives 42 Specificity = 0.666 False positives 3 True negatives 6 Total 87 miR-296 WC bp at nt 2–7 True positives 8 Sensitivity = 0.80 False negatives 2 Specificity = 0.50 False positives 1 True negatives 1 Total 12 WC bp at nt 2–7, and 40% FE threshold (−19.44) True positives 7 Sensitivity = 0.70 False negatives 3 Specificity = 0.50 False positives 1 True negatives 1 Total 12 miR-375 WC bp at nt 2–7 True positives 9 Sensitivity = 0.375 False negatives 15 Specificity = 0.929 False positives 1 True negatives 13 Total 38 WC bp at nt 2–7, and 40% FE threshold (−16.68) True positives 8 Sensitivity = 0.333 False negatives 16 Specificity = 0.929 False positives 1 True negatives 13 Total 38Of 158 genes experimentally tested for regulation by miR-134, 85 occur in our database, as do 14 of 24 tested for regulation by miR-296, and 22 of 44 tested for regulation by miR-375. [score:6]
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[+] score: 13
For example, miR-17-92 cluster are expressed on endothelial cells in addition to cardiomyocytes [40], and miR-296, miR-10b, miR-192 and miR-15a are also expressed on endothelial cells [41]. [score:5]
The remaining 14 (miR-18a-5p, miR-146a-5p, miR-30d-5p, miR-17-5p, miR-200a-3p, miR-19b-3p, miR-21-5p, miR-193-5p, miR-10b-5p, miR-15a-5p, miR-192-5p, miR-296-5p, miR-29a-3p, and miR-133a-3p) were upregulated in HCM patients with T [1] < 470 ms compared with those with T [1] ≥ 470 ms, and 11 (except miR-192-5p, miR-296-5p and miR-133a-3p) were significantly inversely correlated with postcontrast T [1] values. [score:3]
11 miRNAs were significantly and inversely correlated with postcontrast T [1] times, but the inverse correlations with T [1] times were not significant for miR-192-5p (r = 0.246, p = 0.071), miR-296-5p (r = 0.239, p = 0.079) and miR-133a-3p (r = −0.208, P = 0.127) (Fig.   3). [score:1]
T [1] ≥ 470 ms Table 3Correlations between circulating miRNAs measured by miRNA array and T [1] times miRNA r P value miR-18a-5p −0.521 0.082 miR-146a-5p −0.658 0.020 miR-30d-5p −0.599 0.040 miR-17-5p −0.458 0.134 miR-200a-3p −0.436 0.157 miR-19b-3p −0.434 0.159 miR-21-5p −0.443 0.150 miR-193a-5p −0.553 0.062 miR-10b-5p −0.548 0.065 miR-15a-5p −0.475 0.119 miR-192-5p −0.512 0.089 miR-296-5p −0.557 0.060 miR-96-5p −0.579 0.049 miR-373-3p −0.517 0.085 Spearman correlation coefficients were computed to assess the correlations between postcontrast T1 times and miRNAs We validated the expression of the above 14 miRNAs plus miR-29a-3p and miR-133a-3p in all 55 HCM patients by. [score:1]
T [1] ≥ 470 ms Table 3Correlations between circulating miRNAs measured by miRNA array and T [1] times miRNA r P value miR-18a-5p −0.521 0.082 miR-146a-5p −0.658 0.020 miR-30d-5p −0.599 0.040 miR-17-5p −0.458 0.134 miR-200a-3p −0.436 0.157 miR-19b-3p −0.434 0.159 miR-21-5p −0.443 0.150 miR-193a-5p −0.553 0.062 miR-10b-5p −0.548 0.065 miR-15a-5p −0.475 0.119 miR-192-5p −0.512 0.089 miR-296-5p −0.557 0.060 miR-96-5p −0.579 0.049 miR-373-3p −0.517 0.085 Spearman correlation coefficients were computed to assess the correlations between postcontrast T1 times and miRNAs Validation of by real-time PCRWe validated the expression of the above 14 miRNAs plus miR-29a-3p and miR-133a-3p in all 55 HCM patients by. [score:1]
In addition, miR-15a is essential for apoptosis [38], while miR-296 has been named an angiomiR [39]. [score:1]
8 miRNAs (miR-18a-5p, miR-30d-5p, miR-21-5p, miR-193-5p, miR-10b-5p, miR-15a-5p, miR-296-5p, and miR-29a-3p) were selected by the mo del and the AUC for the combination of these 8 miRNAs remained 0.87 (Fig.   4). [score:1]
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The expression of miR-296-5p is abnormally increased in gastric cancer, which inhibits the expression of caudal-related homeobox 1 (CDX1). [score:7]
Furthermore, miR-296-5p/CDX1 affects the phosphorylation level of the extracellular signal-regulated kinases 1 and 2 (ERK1/2) through the mitogen-activated protein kinase (MAPK)/ERK pathway and induces changes in the expression levels of the cell cycle-related protein cyclin D1 and the apoptosis-related proteins B-cell lymphoma 2 (Bcl2) and BCL2 -associated X (Bax), thus maintaining the survival of gastric cancer cells and regulating cell proliferation [55]. [score:5]
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miR-296 targets IKBKE, which is involved in signaling pathways including Toll-like receptor signaling and signal transduction prompting apoptosis [32]. [score:3]
The strongest association was found with PC [20] and hsa-miR-296-5p, as shown in Fig 1. Sensitivity analysis (S1 Table) revealed no significant changes in parameters for the mo dels with the exception of non-significance of hsa-miR-30d. [score:1]
Three novel miRNAs were identified, including our strongest association, miR-296-5p. [score:1]
Of 155 well-detected circulating miRNAs, eight were significantly associated with PC [20] with the strongest association with miR-296-5p. [score:1]
Therefore, miR-296 may attenuate immune response and could modulate AHR via the NFκB pathway. [score:1]
We detected AHR related miRNAs previously associated with asthma, but not PC [20], in addition to a novel association of miR-296, that may have an immunomodulatory effect. [score:1]
Nonetheless, the most significant association was a novel association with miR-296, and this miRNA may be a viable serum biomarker for altered immunity and AHR in pediatric asthmatic patients. [score:1]
Our most significant association was found with hsa-miR-296-5p (Table 2). [score:1]
Representative scatter plot of serum miR-296 cycle threshold and log [2]PC [20] in the CAMP cohort with least squares regression line and 95% confidence interval. [score:1]
0180329.g001 Fig 1Representative scatter plot of serum miR-296 cycle threshold and log [2]PC [20] in the CAMP cohort with least squares regression line and 95% confidence interval. [score:1]
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[+] score: 12
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-139, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-190a, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-429, hsa-mir-491, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, hsa-mir-517a, hsa-mir-500a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-637, hsa-mir-151b, hsa-mir-298, hsa-mir-190b, hsa-mir-374b, hsa-mir-500b, hsa-mir-374c, hsa-mir-219b, hsa-mir-203b
Inverse relationship with its downstream target Stathmin 1. Microtubules stabilization (G1-M transition)Gramantieri et al., 2007, 2008; Jiang et al., 2008; Wong et al., 2008; Liu et al., 2009; Xu et al., 2011; Karakatsanis et al., 2013 miR-224 Promotes proliferation and inhibits apoptosis inhibitor-5 (API-5) transcript expressionMurakami et al., 2006; Meng et al., 2007; Gramantieri et al., 2008; Ladeiro et al., 2008; Li et al., 2008; Wang et al., 2008; Chen, 2009; Huang et al., 2009; Liu et al., 2009; Su et al., 2009; Pineau et al., 2010; Wong et al., 2010 miR-296-5p It is still unknown if contribute to HCC development and tumor progressionBorel et al., 2012b; Katayama et al., 2012; Vaira et al., 2012; Wei et al., 2013b miR-338/-3p Associated with clinical HCC aggressiveness. [score:10]
miR-296 regulation of a cell polarity-cell plasticity module controls tumor progression. [score:2]
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19
[+] score: 12
Other miRNAs from this paper: hsa-mir-188, hsa-mir-328, hsa-mir-331, hsa-mir-432
Down regulation of hsa-miR-296 in ECs inhibits angiogenic responses in cultured ECs. [score:4]
Angiogenic factors can increase the expression of hsa-miR-296. [score:3]
Furthermore, inhibition of hsa-miR-296 with antagomirs reduced angiogenesis in tumor xenografts in vivo. [score:3]
For example, hsa-miR-296 has recently been shown to play a regulatory role in angiogenesis (39). [score:2]
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[+] score: 11
Downregulation of miR-296 causes aberrant expression of its target NUMBL leading to reduced KLF4 -expression and increased random cell migration, invasion and in vivo metastasis [100]. [score:10]
This mechanism may be more general since loss of miR-296 is described in several cancers [101]. [score:1]
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[+] score: 10
Additionally, miRNA profiling in HEV71-infected Vero cells indicated that hsa-miR-296-5p inhibited HEV71 replication by targeting the viral genome [29], and hsa-miR-23b inhibited HEV71 replication through the down-regulation of the HEV71 VP1 protein [30]. [score:10]
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[+] score: 10
A study by Xun et al. show that the expression level of miR-4530 [72] and miR-296-5p are most differentially up-regulated in enterovirus 71 (EV71) infections [73]. [score:6]
Additionally, Zheng et al. showed that miR-296-5p supressed EV71 replication by targeting the viral genome [73]. [score:3]
Indeed, some miRNAs that have been previously linked to carcinogenesis of different organs and tissues, such as miR-2861 [47, 48], miR-4530 [49], miR-638 [50], miR-371b-5p [51], miR-1225-5p [52, 53], miR-296-5p [54, 55], miR-4787-5p [56], miR-4281 [57], miR-4455 [58], miR-197-3p [59], miR-369-5p [60, 61] and miR-505-3p [62] which were found to be altered in brucellosis in our analysis. [score:1]
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23
[+] score: 10
MicroRNAs also play a role in the maintenance of stem cells, and some are expressed during self-renewal (miR-269, miR-290-295 cluster, miR-371, miR-200c) while others are up-regulated during differentiation (miR-21, miR-22, miR-29, miR-134, miR-296, miR-470) (see text for details). [score:6]
In particular, miR-134, miR-296 and miR-470 are up regulated during the differentiation of mouse embryonic stem cells induced by retinoic acid, and target these three transcription factors. [score:4]
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[+] score: 10
Other miRNAs from this paper: hsa-mir-874
A comparison between the miRNAs expression profile of OID daughters and their fathers revealed that three miRNAs were similarly altered in both generations (Fig. 5c): mmu-miR-1896, mmu-miR-874 and mmu-miR-296-5p were down-regulated in paternal sperm and their female offspring’s mammary tissue. [score:6]
In addition, a list of canonical pathways generated using predicted targets for each individual miRNA is provided in Table S6 (mmu-miR-1896), Table S7 (mmu-miR-874), and S8 (mmu-miR-296-5p). [score:3]
We focused our down-stream analyses on mmu-miR-1896, mmu-miR-874 and mmu-miR-296-5p. [score:1]
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25
[+] score: 9
In GC, oncogenic miRNAs such as miR-21 [12], miR-362 [13] and miR-296-5p [14] are abnormally upregulated, and tumor suppressing miRNAs such as miR-506 [15], miR-129-5p [16] and miR-361-5p [17] are significantly downregulated. [score:9]
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[+] score: 8
RT-qPCR was performed to evaluate the expression levels of hsa_circ_0043497 (A) and its top 5 predicted miRNA targets (miR-335-3p, miR-186-5p, miR-380-5p, miR-296-3p and miR-522-3p) (B), hsa_circ_0001204 (C) and its top 5 predicted miRNA targets (miR-612, miR-657, miR-362-3p, miR-377-3p and miR-136-5p) (D) in ten human MDMs after 24 h of infection with H37Rv. [score:5]
The potential miRNAs targets of hsa_circ_0043497 include miR-335-3p, miR-186-5p, miR-380-5p, miR-296-3p and miR-522-3p. [score:3]
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[+] score: 8
In the first group, there were 19 miRNAs with an expression level that was four times higher in BCSCs than in MCF-7 cells: miR-122a, miR-152, miR-212, miR-224, miR-296, miR-31, miR-373*, miR-489, PRED_MIR127, PRED_MIR154, PRED_MIR157, PRED_MIR162, PRED_MIR165, PRED_MIR191, PRED_MIR207, PRED_MIR219, PRED_MIR246, PRED_MIR88 and PRED_MIR90. [score:3]
We performed real-time RT-PCR for 10 miRNAs: miR-122a, miR-188, miR-200a, miR-21, miR-224, miR-296, miR-301, miR-31, miR-373* and miR-200C. [score:1]
Eight of the nine miRNAs tested by real-time RT-PCR gave results consistent with the microarray data, except miR-296, indicating a concordance rate of 88.89% (C). [score:1]
The analysed miRNAs included miR-122a, miR-188, miR-200a, miR-21, miR-224, miR-296, miR-301, miR-31, miR-373* and miR-200C. [score:1]
Eight of the ten miRNAs tested gave real-time RT-PCR results that were concordant with the microarray data, with miR-296 being the only exception, indicating a concordance rate of 88.89%. [score:1]
Moreover, miR-301, miR-296, miR-21 and miR-373* have been reported to be expressed in human embryonic stem cells and other stem cells, indicating that these miRNAs may play a constitutive role in maintaining the biological characteristics of stem cells [40, 41]. [score:1]
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[+] score: 8
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
expression increases in mouse ESCs treated with retinoic acid (RA), favoring ESCs differentiation into ectodermal lineages including neural cells by directly regulating the expression of the pluripotency factors Nanog and Sox2 and indirectly Oct4 in combination with miR-296 and miR-470 (Tay et al., 2008; Niu et al., 2013). [score:8]
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[+] score: 8
Subsequent RT-qPCR validated upregulated expression of miR-182, miR-488, miR-292, and miR-296, while miR-200a was downregulated in the mo del group compared to controls [32]. [score:8]
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[+] score: 7
Of these 16 miRNAs, 9 were downregulated (let-7d, miR-106b, miR-122a, miR-141, miR-183, miR-195, miR-200a, miR-335, mir424) and 7 were upregulated (miR-100, miR-199a, miR-296, miR-29a, miR-29c, miR-99a, mir-494). [score:7]
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[+] score: 7
On the other hand, differentiation-related miRNAs (i. e., miR-296, miR-470) can inhibit the expression of the core transcription factors, creating a mutually-exclusive loop of developmental- or pluripotency-related regulators (reviewed in [94]). [score:7]
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[+] score: 7
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, hsa-mir-215, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-mir-15b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-141, hsa-mir-143, hsa-mir-152, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-184, hsa-mir-200c, hsa-mir-155, hsa-mir-29c, hsa-mir-200a, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-342, hsa-mir-148b, hsa-mir-451a, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-15b, ssc-mir-184, ssc-mir-224, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-let-7f-1, ssc-mir-103-1, ssc-mir-21, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-671, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-16b, bta-mir-21, bta-mir-499, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-27b, bta-mir-31, bta-mir-15b, bta-mir-215, bta-mir-30e, bta-mir-148b, bta-mir-192, bta-mir-200a, bta-mir-200c, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-10b, bta-mir-24-2, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-mir-342, bta-let-7f-1, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-15a, bta-mir-99b, hsa-mir-664a, ssc-mir-99b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, bta-mir-141, bta-mir-143, bta-mir-146a, bta-mir-152, bta-mir-155, bta-mir-16a, bta-mir-184, bta-mir-24-1, bta-mir-223, bta-mir-224, bta-mir-26a-1, bta-mir-296, bta-mir-29d, bta-mir-378-1, bta-mir-451, bta-mir-486, bta-mir-671, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, ssc-mir-181a-1, ssc-mir-215, ssc-mir-30a, bta-mir-2318, bta-mir-2339, bta-mir-2430, bta-mir-664a, bta-mir-378-2, ssc-let-7a-1, ssc-mir-378-1, ssc-mir-29a, ssc-mir-30e, ssc-mir-499, ssc-mir-143, ssc-mir-10b, ssc-mir-486-1, ssc-mir-152, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-99a, ssc-mir-148b, ssc-mir-664, ssc-mir-192, ssc-mir-342, ssc-mir-125b-1, oar-mir-21, oar-mir-29a, oar-mir-125b, oar-mir-181a-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-296, ssc-mir-155, ssc-mir-146a, bta-mir-148c, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-664b, hsa-mir-378j, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-31, ssc-mir-671, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, oar-let-7a, oar-let-7f, oar-mir-103, oar-mir-10b, oar-mir-143, oar-mir-148a, oar-mir-152, oar-mir-16b, oar-mir-181a-2, oar-mir-200a, oar-mir-200b, oar-mir-200c, oar-mir-23a, oar-mir-26a, oar-mir-29b-1, oar-mir-30a, oar-mir-99a, bta-mir-664b, chi-let-7a, chi-let-7f, chi-mir-103, chi-mir-10b, chi-mir-125b, chi-mir-126, chi-mir-141, chi-mir-143, chi-mir-146a, chi-mir-148a, chi-mir-148b, chi-mir-155, chi-mir-15a, chi-mir-15b, chi-mir-16a, chi-mir-16b, chi-mir-184, chi-mir-192, chi-mir-200a, chi-mir-200b, chi-mir-200c, chi-mir-215, chi-mir-21, chi-mir-223, chi-mir-224, chi-mir-2318, chi-mir-23a, chi-mir-24, chi-mir-26a, chi-mir-27b, chi-mir-296, chi-mir-29a, chi-mir-29b, chi-mir-29c, chi-mir-30a, chi-mir-30e, chi-mir-342, chi-mir-378, chi-mir-451, chi-mir-499, chi-mir-671, chi-mir-99a, chi-mir-99b, bta-mir-378d, ssc-mir-378b, oar-mir-29b-2, ssc-mir-141, ssc-mir-200b, ssc-mir-223, bta-mir-148d
Similarly, Naeem et al. (2012) demonstrated a differential regulation of four miRNAs (Bta-miR-181a, miR-16, miR-31, and miR223) in bovine mammary tissue infected with Streptococcus uberis as compared to healthy tissue while Hou et al. (2012) showed that bta-miR-296, miR-2430, and miR-671 were up-regulated and miR-2318 was down-regulated in mammary tissues of cows with mastitis. [score:7]
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[+] score: 7
Zheng et al (21) showed that miRNA-296-5p suppressed EV71 replication in host cells by inhibiting two potential targets (2,115-2,135 nt and 2,896-2,920 nt) located in the EV71 genome. [score:7]
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[+] score: 7
Among miRNA analyzed, miR-23b, miR-30d, miR-132, miR-140-3p, miR-145, miR-150, miR-204 were up-regulated in OA chondrocytes whereas miR-22, miR-25, miR-26, miR-30c, miR-92b, miR-127, miR-194, miR-197, miR-296-5p, miR-342-3p, miR-488 were down-regulated in OA chondrocytes (Figure  1B). [score:7]
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35
[+] score: 7
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Some miRNAs (miR-129-1-3p; miR-129-2-3p, miR-129-5p, miR181c-5p, miR181d-5p, miR-409a-5p, miR-655 and miR-874-3p) were up-regulated (Fig. 2, Supplementary Fig. S3A), whereas others (miR-296-5p, miR-500-3p and miR-652-3p) were down-regulated only in the chronic phase, while not being significantly altered during latency (Fig. 2, Supplementary Fig. S3B). [score:7]
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[+] score: 7
In contrast, when BBR was combined with NVP-AUY922, the growth of the normally resistant cells was reduced which was mediated by miR-296-5p -mediated suppression of the Pin1/beta-catenin/cyclinD1 signaling pathway and inhibition of CDK4 expression [252]. [score:7]
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37
[+] score: 6
The inflammatory miRNA miR-146b-3p, miR-101 and the cell survival miRNA miR-193a-3p and miR-296-5p were only found differentially expressed in macrophages of active TB group, suggesting response that alters macrophage survival in the infected host. [score:3]
Interestingly, hsa-miR-146b-3p and hsa-miR-296-5p were expressed in all of LTBI group but not in the active MTB and healthy controls. [score:3]
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38
[+] score: 6
Other miRNAs from this paper: hsa-mir-221, hsa-mir-134
Through targeting the core stemness factors such as Oct4, Nanog, and Sox2, the up- and down-regulation of miRNAs including miR134, miR296, and miR470, plays roles in modulating the self-renewal, pluripotency, and differentiation of ESCs [35]. [score:6]
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[+] score: 6
Five miRNAs (hsa-miR-130a*, hsa-miR-296-5p, hsa-miR-493*, hsa-miR-520d-3p, hsa-miR-661) had different expression levels between latent TB and healthy controls; all of them except hsa-miR-296-5p were up-regulated in healthy controls. [score:6]
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40
[+] score: 6
Smoking was associated with the down-regulation of 27 plasma miRNAs (Fig.   7), including several previously identified as performing tumour suppressor-like functions; let-7i-5p [2], miR-148a-5p [22], miR-218-5p [17], miR-29-3p [20], miR-133a [4], miR-296-5p [10] and miR-370 [21]. [score:6]
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41
[+] score: 6
B. Real-time PCR further revealed that human miR-221-3p, miR-409-5p, miR-1290, miR-155-5p, miR-31-3p, miR-7-5p, miR-362-5p, miR-493-5p, miR-296-5p, and miR-199b-5p were statistically expressed at lower levels in Sertoli cells of SCOS patients than Sertoli cells of OA patients. [score:3]
In contrast, hsa-miR-221-3p, hsa-miR-409-5p, hsa-miR-1290, hsa-miR-155-5p, hsa-miR-31-3p, hsa-miR-7-5p, hsa-miR-362-5p, hsa-miR-493-5p, hsa-miR-296-5p, and hsa-miR-199b-5p were statistically downregulated in human Sertoli cells of SCOS patients compared to OA patients (Figure 3B). [score:3]
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42
[+] score: 6
OS upregulates a group of miRNAs (miR-329, miR-193b, miR-20a, miR-296, and miR-130b), which is associated with affecting 83 target genes. [score:6]
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43
[+] score: 6
miR-125b was consistently downregulated upon cocaine treatment, whereas expression of other miRNAs (miR-26, miR-150, miR-223, miR-122, and miR-296) were not significantly affected. [score:6]
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44
[+] score: 5
Out of 12 miRNA families that were predicted to target the PRKAG1 sense promoter in both human and mouse, nine (miR-718, miR-1224, miR-188, miR-346, miR-296, miR-671, miR-221, miR-1306, miR-506) can form highly stable duplex structures with their target sites (MFE ≤ −30 kcal/mol) in both organisms. [score:5]
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45
[+] score: 5
Zheng et al. provned that hsa-miR-296-5p suppressed EV71 replication by targeting the viral genome [17]. [score:5]
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46
[+] score: 5
[43] Hypoxia induced by PDT induces miR-210 expression, followed by an increased expression of both VEGF and miR-296. [score:5]
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47
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-198, hsa-mir-129-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-196a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-382, hsa-mir-383, hsa-mir-151a, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, hsa-mir-325, hsa-mir-196b, hsa-mir-424, hsa-mir-20b, hsa-mir-429, hsa-mir-451a, hsa-mir-409, hsa-mir-412, hsa-mir-376b, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-181d, hsa-mir-499a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-301b, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j
In rat thyroid cells, many miRNAs such as miR-1, miR-28a, and miR-296-3p are differentially expressed and possibly they target transcripts that are important in thyroid cell proliferation (Leone et al. 2011). [score:5]
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48
[+] score: 4
A role for miR-296 in the regulation of lipoapoptosis by targeting PUMA. [score:4]
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49
[+] score: 4
The results indicated that a subset of miRNAs, including miR-4270, miR-4689, miR-296-5p, miR-3619-3p, miR-4731-3p, and miR-4442, was significantly down-regulated in KRAS [G12V] transfected cells. [score:4]
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[+] score: 4
In contrast, seven of the apoptosis -associated miRNAs, including miR-153, miR-155, miR-182, miR-202, miR-204, miR-296 and miR-337, were obviously down-regulated. [score:4]
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51
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-296, mmu-mir-298, mmu-mir-34c, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, hsa-mir-330, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-519d, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-501, mmu-mir-718, mmu-mir-18b, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Six miRNAs showed a trend for a stronger upregulation during the brown adipocyte differentiation - miRPlus_17856, mmu-miR-381, mmu-miR-501-3p, mmu-miR-21*, mmu-miR-296-5p and miRPlus_17832. [score:4]
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[+] score: 4
Besides, we also found that miRNA-296 have a very high expression level in HepG2/DOX cells. [score:3]
01 Down 4.40E-07 hsa-miR-4488 5.95 Up 4.10E-35 hsa-miR-1269b −6.74 Down 3.15E-06 hsa-miR-296-5p 5.84 Up 3.88E-78 hsa-miR-3674 −6.74 Down 3.16E-06 hsa-miR-4454 5.19 Up 3.07E-85 hsa-miR-3910 −6.74 Down 3.17E-06 hsa-miR-4687-3p 4.37 Up 8.32E-26 hsa-miR-642a-3p −6.74 Down 5.10E-32 hsa-miR-3654 3.38 Up 1.21E-25 hsa-miR-486-5p −6.46 Down 2.81E-100 hsa-miR-577 2.94 Up 8.64E-05 hsa-miR-203 −6.30 Down 3.19E-89 hsa-miR-4508 2.9 Up 5.94E-06 hsa-miR-1277-3p −6.16 Down 3.01E-41 hsa-miR-3687 2.49 Up 2.04E-05 hsa-miR-1277-5p −5. [score:1]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-31, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-30c-2, hsa-mir-147a, hsa-mir-10a, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-204, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-219a-2, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302d, hsa-mir-374a, hsa-mir-375, hsa-mir-378a, hsa-mir-330, hsa-mir-328, hsa-mir-342, hsa-mir-325, hsa-mir-424, hsa-mir-429, hsa-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-497, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520b, hsa-mir-520c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-450a-2, hsa-mir-503, hsa-mir-608, hsa-mir-625, hsa-mir-629, hsa-mir-663a, hsa-mir-1271, hsa-mir-769, hsa-mir-378d-2, hsa-mir-675, hsa-mir-147b, hsa-mir-374b, hsa-mir-663b, hsa-mir-378b, hsa-mir-378c, hsa-mir-374c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-4661, hsa-mir-219b, hsa-mir-203b, hsa-mir-378j, hsa-mir-486-2
miR-204 and miR-296-5p presented the greatest down-regulation in response to dietary zinc depletion. [score:4]
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[+] score: 4
Top 10 up-regulated miRNAs with maximum score and high fold change were: miR-317-5p, miR-373, miR-1268, miR-191*, miR-150, miR-1275, miR-188-5p, miR-1238, miR-134 and miR-296-5p. [score:4]
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55
[+] score: 3
For instance, miR-134, miR-296 and miR-470 target the core transcription factor trio, Oct4, Sox2 and Nanog [95]. [score:3]
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56
[+] score: 3
Liu et al. used liposome based nanoparticles to deliver anti-miR-296 for inhibiting blood vessel formation in cancer cells [144]. [score:3]
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57
[+] score: 3
Other miRNAs from this paper: hsa-mir-187, hsa-mir-155
Also, miR-296 was reported to be a critical upstream regulator of S100A4 and the dysregulation of the miR-296/S100A4 axis promoted EMT by the alteration of the EMT-related proteins [76]. [score:3]
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58
[+] score: 3
Lee H. Hwang S. J. Kim H. R. Shin C. H. Choi K. H. Joung J. G. Kim H. H. Neurofibromatosis 2 (NF2) controls the invasiveness of glioblastoma through YAP -dependent expression of cyr61/ccn1 and miR-296-3pBiochim. [score:3]
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[+] score: 3
MiR-296 levels are elevated in primary human brain microvascular endothelial cells, likely by glioma cell-derived vascular growth factors, and act as a promoter of angiogenesis by targeting hepatocyte growth factor-regulated tyrosine kinase substrate, a protein mediating the degradation of the growth factor receptors VEGFR2 and PDGFRβ [104]. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-17, hsa-mir-19a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-198, hsa-mir-208a, hsa-mir-10a, hsa-mir-223, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-155, hsa-mir-29c, hsa-mir-99b, hsa-mir-196b, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-640, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-550a-3, bta-mir-29a, bta-mir-125b-1, bta-mir-126, bta-mir-10a, bta-mir-124a-1, bta-mir-17, bta-mir-29b-2, bta-mir-29c, bta-mir-150, bta-mir-122, bta-mir-125b-2, bta-mir-19a, bta-mir-99b, hsa-mir-208b, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, bta-mir-124a-2, bta-mir-124b, bta-mir-146a, bta-mir-155, bta-mir-196b, bta-mir-208a, bta-mir-208b, bta-mir-223, bta-mir-296, bta-mir-29d, bta-mir-9-1, bta-mir-9-2, bta-mir-29e, bta-mir-29b-1, hsa-mir-548q, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, bta-mir-2284w, bta-mir-2284x, hsa-mir-548y, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, hsa-mir-548ay, hsa-mir-548az, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
Reference miRNA Tissue Source Condition(31) Genome-wide embryo, thymus, lymph node, and small intestine Holstein–Friesian None(44) Genome-wide Bos taurus kidney cells (MDBK) Cell line Bovine herpesvirus 1(46) miR-10a, -15b, 16a, -17, -21, 31, -145, 146a, 146b, 155, -181a, -205, -221, and -223 Mammary tissue Holstein–Friesian Mastitis(48) miR-223 Venous blood Holstein–Friesian Mastitis(45) miR-9, -125b, -155, -146a, and -223CD14 monocytes ex vivo Holstein–Friesian LPS and SEB(49) miR-296, -2430, -671, and -2318 Mammary tissue Holstein–Friesian Mastitis(39) miR-17-5p, -20b, and -93 Mammary tissue Holstein–Friesian Mastitis(40) Genome-wideMammary epithelial cells ex vivo Holstein–Friesian Mastitis(41) Genome-wide Alveolar macrophages Holstein–Friesian None(39) Genome-wide Peripheral blood Holstein–Friesian Mastitis(42) Genome-wide CD14 monocytes Holstein–Friesian Mastitis(47) Genome-wide MAC-T cells Cell lineHeat-inactivated E. coli or S. aureus More recent studies have employed high-throughput sequencing approaches to temporally profile genome-wide changes in miRNA expression in different cell-types in response to challenge with bovine mastitis-causing pathogens such as Escherichia coli, S. aureus, and S. uberis. [score:3]
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In a more technically advanced study, targeted nanoparticles decorated with a cyclic RGD peptide were used to deliver exogenous miR-296 to tumour vasculature in vivo, resulting in a significant decrease in microvessel formulation 36. [score:3]
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miR-296–3p expression also decreased after FO compared with the SO and PO diets. [score:2]
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63
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The MoR plot illustrates the 9 most informative miRNAs, hsa-miR-505-5p, hsa-miR-4467, hsa-miR-766, hsa-miR-375, hsa-miR-708, hsa-miR-3622b-3p, hsa-miR-296, hsa-miR-219 and hsa-miR-103, each reaching a MoR value ≥ 0.57 (critical MoR value on the information chain). [score:1]
Moreover, we could also confirm the 9 informative miRNAs (miR-505-5p, miR-4467, miR-766, miR-375, miR-708, miR-3622b-3p, miR-296, miR-219 and miR-103) from set B as significant biomarkers by MANCOVA all reaching Bonferroni corrected significance. [score:1]
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64
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In triplicate, select miRs were compared against undifferentiated hESCs as well as the 4 endogenous controls, nucleolar RNAs RNU38B and RNU48 (as recommended by the array manufacturer) and the stably expressed miRs, miR-188 and miR-296-5p (as identified in our own experiments) (Figure 1D). [score:2]
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Many miRNAs were reported to be associated with GC development in the past decade, including miR-146a (Yao et al., 2013), miR-204-5p (Zhang et al., 2015), miR-486 (Oh et al., 2011), miR-192 (Jin et al., 2011), miR-215 (Jin et al., 2011), miR-34b/c (Suzuki et al., 2010), miR-29a (Cui et al., 2011), miR-409-3p (Li et al., 2012a), and miR-296-5p (Li et al., 2014). [score:2]
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66
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miR-23 and miR-296 seed matches are indicated. [score:1]
Expanding our miRNA site search beyond the 87 miRNA families conserved beyond mammals to the 66 miRNA families conserved only within the mammalian lineage (Figure S9A in Additional file 12), we found that circRNA-ZNF91 had 39 additional sites for miR-296 (Figure  6E). [score:1]
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67
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[111] ↑ miR-155; miR-7 IL4-DCs (Setting 3)IFN-α/ β TNF α/ PGE [2]/ IFN-α/βSTAT1STAT4[62] pDCs IFN-α↑ miR-155 miR-155 *[114] pDCs IFN-α/β ↑ miR-146a[115] IFN-DCs (Setting 1) IFN-α/ω IFN-βCXCL11FCGR, MARCO, CLEC5A, DEFB1, IDO1[32] MDMs IFN-α/β ↑ miR-28; miR-125b; miR-150; miR-382[116] IFN-DCs (Setting 1) IFN-α LOX-1[40] IL4-DCs (Setting 3) RSV/ IFN-β * ↑ miR Let7b[117] IFN-DCs (Setting 1) IFN-α TLR7[27] PBMCs Type I IFNs ↑ miR146a[118] IFN-DCs (Setting 1) IFN-α TRAIL, granzymes, KLRs and other NK cell receptors, DCLAMP, CCR7 and CD49d[26] PBMCs MS/ IFN-β ** ↓ mir-29 family[119] IFN-DCs (Setting 1) IFN-β IL-6, IL-1β, IL-10, CCL20, CCL3, CCL5, CXCR4, CCR5, CCR2,CD44, TLR2, TLR4, CLECSF12, PRG1, TAP1, β2 microglobulin, CD74, CD1a, CD68 LAMP-3, NFkB2, SOD2, Cdc42, IFIT1[31] PBMCs (healthy donors) IFN-α ↑ miR-1; miR-30; miR-128; miR-196; miR-296;[120] PBMCs (CHC) IFN-α ** ↑ miR-1; miR-30; miR-296; Notes: A summary of representative type I IFN modulated genes (left column) or miR (right column). [score:1]
In the context of antiviral response, it has been reported that several IFN -induced miR (miR-1, miR-30, miR-128, miR-196, miR-296) are basally present as well as induced by type I IFNs to varying degrees in PBMCs from healthy individuals and from chronic human HCV-infected patients [120]. [score:1]
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MiR-92a (19), miR-103/107 (20), miR-21, miR143, miR145, miR-205 (21) and miR-296 (22), among others, have been confirmed to be involved in the development of ESCC. [score:2]
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69
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Third, we chose several miRNAs which had potentially problematic sequences or exhibited atypical behavior during the development of the Agilent microarray platform: two of these did not show as good a linear titration curve as other miRNAs tested in a previous study (miR-126*, miR-296) [26], and two other miRNAs were previously reported not to be labeled by enzymatic methods similar (but not identical) to that used with the Agilent microarray assay (miR-208, miR-219) [33]. [score:1]
Scatter plots are shown for titration of synthetic miR-296 into liver (top left panel) and placenta (top right panel) total RNAs, and miR-494 into liver (lower left) and placenta (lower right) total RNAs. [score:1]
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70
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They also found that EVs from EPCs contained the and miR-296 and that these miRNAs contributed to the angiogenesis properties, suggesting that EVs from EPCs activate an angiogenic program in islet endothelium (Cantaluppi et al., 2012a). [score:1]
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71
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miR-296 44.8Angiogenesis [41]. [score:1]
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72
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The renoprotective effect was lost if microvesicles were pre -treated with RNAse, or if the pro-angiogenic microRNAs, miR-126 and miR-296, were depleted. [score:1]
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hsa-let-7a hsa-miR-296 hsa-miR-125b hsa-miR-183 hsa-miR-19b hsa-miR-30b hsa-miR-30c hsa-miR-30a-5p hsa-miR-30d hsa-miR-27a hsa-miR-103 hsa-miR-107 hsa-miR-92 hsa-miR-10a hsa-miR-326 Table 3 shows an overview of predictions on 39,215 3'UTR sequences in human genome and on 15 other genomes. [score:1]
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74
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In the cerebellum, novel_circRNA_007362 was predicted to combine with 24 miRNAs (tch-let-7e-5p, tch-let-7i-5p, tch-let-7f-5p, tch-miR-125a-5p, tch-miR-1301, tch-miR-135a-5p, tch-miR-135b-5p, tch-miR-15b-5p, tch-miR-195-5p, tch-miR-1-5p, tch-miR-218-5p, tch-miR-22-3p, tch-miR-26a-5p, tch-miR-26b-5p, tch-miR-296-3p, tch-miR-335-5p, tch-miR-34a-5p, tch-miR424-5p,tch-miR-491-5p, tch-miR-455-3p,tch-miR-503, tch-miR-592, tch-miR-9771e, and tch-miR-98-5p). [score:1]
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75
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-23a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-218-1, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-128-1, hsa-mir-145, hsa-mir-191, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-30c-1, hsa-mir-99b, hsa-mir-30e, hsa-mir-361, hsa-mir-337, hsa-mir-148b, hsa-mir-196b, hsa-mir-425, hsa-mir-20b, hsa-mir-486-1, hsa-mir-488, hsa-mir-181d, hsa-mir-498, hsa-mir-519c, hsa-mir-520a, hsa-mir-526b, hsa-mir-520d, hsa-mir-506, hsa-mir-92b, hsa-mir-608, hsa-mir-617, hsa-mir-625, hsa-mir-641, hsa-mir-1264, hsa-mir-1271, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-30d, bta-mir-128-1, bta-mir-145, bta-mir-181a-2, bta-mir-30b, bta-mir-181b-2, bta-mir-20b, bta-mir-30e, bta-mir-92a-2, bta-let-7d, bta-mir-148b, bta-mir-181c, bta-mir-191, bta-mir-210, bta-mir-23a, bta-mir-361, bta-mir-425, bta-let-7g, bta-mir-30a, bta-let-7a-1, bta-let-7f-1, bta-mir-30c, bta-let-7i, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-99b, hsa-mir-890, hsa-mir-888, hsa-mir-889, hsa-mir-938, hsa-mir-1184-1, hsa-mir-1203, hsa-mir-1204, hsa-mir-1265, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-218-1, bta-mir-296, bta-mir-30f, bta-mir-486, bta-mir-488, bta-mir-92a-1, bta-mir-92b, bta-mir-1271, bta-mir-181a-1, bta-mir-181b-1, bta-mir-148c, hsa-mir-1184-2, hsa-mir-1184-3, hsa-mir-486-2, bta-mir-1264, bta-mir-148d
However, 29 miRNAs such as miR-890*, miR-296-5p, miR-617, miR-181c*, miR-889, miR-520a-5p and miR-641 were absent in SE but these miRNAs were detected in HE and CE animals (Fig.   6). [score:1]
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In particular, quercetin, hesperidin, narangin, anthocyanins, catechins, proanthocyanin, caffeic acid, ferulic acid, and curcumin, act through a common mechanism envisaging the modulation of five miRs, i. e., miR-30c, miR-291b-5p, miR-296-5p, miR -373, and miR-467b [179]. [score:1]
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77
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miR-126 and miR-296 have been identified in microvesicles from endothelial progenitor cells and are thought to exert renoprotective effects via their abilities to decrease apoptosis and leukocyte infiltration, while promotes angiogenesis and tubular cell proliferation [43]. [score:1]
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78
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Fu Q miRomics and proteomics reveal a miR-296-3p/PRKCA/FAK/Ras/c-Myc feedback loop modulated by HDGF/DDX5/β-catenin complex in lung adenocarcinomaClin. [score:1]
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79
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These genes have been shown to be silenced by various miRNAs, such as miR-134, miR-145, miR-296 and miR-470 [18]. [score:1]
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80
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Other miRNAs from this paper: hsa-mir-21, hsa-mir-126, hsa-mir-200c, hsa-mir-375
We found in EVs the presence of the islet specific miRNA miR-375 and of the so called “angiomiRs” which are known to promote angiogenesis (miR-126 and miR-296) (Table 2). [score:1]
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81
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Namely, we selected miR-16, miR-21, miR-23a, miR-24, miR-26a, miR-106, miR-141, miR-155, miR-196a, miR-200a, miR-200b, miR-200c, miR-221, miR-222, miR-296-5p, miR-376a, miR-429 and let-7i for this study. [score:1]
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82
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4427975-002623), and miR-296 (Cat. [score:1]
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83
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Several of them have been reported to be involved in EC functions (miR-139 [36] and miR-663 37, 38) or in angiogenesis (miR-483 [39], miR-708 [40], miR-205 [41] and miR-296 [42]). [score:1]
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