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58 publications mentioning hsa-mir-188

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-188. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 366
Overexpression of miR-188 inhibits cell proliferation and G [1]/S transition by directly targeting the expression of multiple cyclin/CDKs complexes, including CCND1, CCND3, CCNE1, CCNA2, CDK2 and CDK4. [score:10]
Moreover, studies in xenograft mouse mo del reveal that miR-188 is capable of inhibiting tumor initiation and progression by suppressing target genes expression and Rb phosphorylation. [score:9]
MiR-188 inhibits both mRNA and protein expression of CCND1, CCND3, CCNE1, CCNA2, CDK4 and CDK2, suppresses Rb phosphorylation and downregulates E2F transcriptional activity. [score:9]
It has been reported that miR-188 is upregulated by the induction of long-term potentiation (LTP) and it serves to fine-tune synaptic plasticity by targeting neuropilin-2 (Nrp-2) expression in the nervous system [35]. [score:8]
Therefore, we concluded that miR-188 inhibits target-gene expression through direct interaction with their 3′UTRs. [score:8]
Since we have shown that miR-188 downregulates the expression of Cyclin D/CDK4 and Cyclin E/CDK2 complexes, we wanted to ask whether overexpression of miR-188 would have an impact on Rb phosphorylation. [score:8]
MiR-188 mediated downregulation of G [1]/S CDKs suppresses Rb phosphorylation and E2F transcriptional activity, and finally leads to G [1]/S cell cycle arrest and growth inhibition. [score:7]
By suppressing the activation of G [1]/S related Cyclin/CDKs, miR-188 suppresses Rb phosphorylation and subsequent activation of E2F transcription factor, which leads to G [1]/S cell cycle arrest and growth inhibition in cancer cells (Figure  6). [score:7]
The expression level of miR-188 also inversely correlates with the expression of miR-188 targets in human nasopharyngeal carcinoma (NPC) tissues. [score:7]
The expression of miR-188 also inversely correlates with expression of its targets in NPC tissues. [score:7]
To define the clinical relevance of our findings that miR-188 suppressed the expression of G [1]/S related cyclin/CDKs, we showed that miR-188 expression was possibly associated with human nasopharyngeal carcinoma. [score:7]
Namely, we examined the expression of miR-188 and its target genes in NPC tissues using qRT-PCR, and an inverse correlation between miR-188 and CCND1, CCNA2, CCND3, CCNE1, CDK2 or CDK4 expression was identified in patient samples (Figure  2E). [score:7]
These results provide strong evidence that miR-188 suppresses tumor initiation and progression in vivo, potentially through downregulation of multiple genes involved in G [1]/S transition. [score:6]
Thus, we speculated that overexpression of miR-188 would lead to a downregulation of E2F transcriptional activity. [score:6]
Therefore, these results suggest that miR-188 inhibits cell proliferation, potentially via downregulation of multiple cyclin/CDK complexes involved in G [1]/S transition. [score:6]
Figure 4 MiR-188 regulates target genes expression through direct binding to their 3′UTRs. [score:6]
The expression of miR-188 target genes of each tumor was detected by western blot. [score:5]
Overexpression of miR-188 inhibits cell proliferation, tumor colony formation and G [1]/S cell cycle transition in human nasopharyngeal carcinoma CNE cells. [score:5]
To test whether silencing endogenous miR-188 would affect target gene expression, we transfected cells with miR-188 antisense oligonucleotides (ant-188). [score:5]
Thus, the in vitro and in vivo results further demonstrate that miR-188 targets the expression of multiple G [1]/S related cyclin/CDKs. [score:5]
Similarly, western blot experiments demonstrated that the protein levels of these genes were significantly suppressed to various degrees by miR-188 overexpression in both transiently and stably transfected cells (Figure  2C, Additional file 3: Figure S2A, B). [score:5]
In order to figure out the potential targets of miR-188, we used Targetscan [61] (http://www. [score:5]
Densitometric analysis of miR-188 target genes expression. [score:5]
MiR-188 suppresses cyclin D/CDK4, cyclin E/CDK2 and cyclin A/CDK2 activity by directly targeting their 3′UTRs. [score:5]
Stable expression of miR-188 inhibits G [1]/S transition and Rb phosphorylation. [score:5]
Through targeting multiple cyclin/CDK complexes, miR-188 blocks G [1]/S transition, suppresses Rb phosphorylation and E2F transcriptional activity. [score:5]
Overexpression of miR-188 suppresses cancer cell proliferation. [score:5]
To investigate the potential targets of miR-188, we searched the genome using miRNA target prediction algorithms, Targetscan and Findtar. [score:5]
These results suggest that miR-188 downregulates CDK -mediated Rb phosphorylation and subsequent activation of E2F. [score:4]
In this study, we demonstrate that miR-188 exerts anti-cancer potential via downregulating multiple G [1]/S related genes, including CCND1, CCND3, CCNE1, CCNA2, CDK2 and CDK4. [score:4]
This study demonstrates that miR-188 exerts anticancer effects, via downregulation of multiple G [1]/S related cyclin/CDKs and Rb/E2F signaling pathway. [score:4]
Taken together, our data highlight the anti-cancer potential of miR-188 and provide a novel mechanism whereby miR-188 controls cell cycle progression via downregulation of multiple cyclin/CDK complexes involved in G [1]/S transition. [score:4]
Recent studies also show that miR-188 is upregulated in UVB-irradiated mouse skin and human nasopharyngeal carcinoma CNE cells under hypoxic stress [36, 37]. [score:4]
Since cell growth and cell proliferation are highly associated with cell cycle regulation, we analyzed 23 of the genes in the cell cycle pathway and identified a series of cyclins and CDKs involved in G [1]/S transition that could be potential miR-188 targets (Figure  1G right panel). [score:4]
MiR-188 Cell cycle G [1]/S transition CDK Cyclin Rb E2F MicroRNAs (miRNAs) are a class of small non-coding RNAs that negatively regulate gene expression at the post-transcriptional level [1]. [score:4]
It has been shown that miR-188 is upregulated in UVB-irradiated mouse skin and human nasopharyngeal carcinoma CNE cells under hypoxic stress. [score:4]
Using bioinformatics approach, we identify a series of genes regulating G [1]/S transition as putative miR-188 targets. [score:4]
The 3′ UTRs of CCND1, CCND3, CDK4, CCNA2, CDK2 and CCNE1 containing predicted targets of miR-188 and their corresponding mutants were amplified from reverse transcribed cDNA and cloned to pmirGLO Dual-Luciferase reporter vector (Promega, E1330). [score:3]
We selected two stable clones in which the expression of miR-188 was nearly 4 folds higher than the negative control (Additional file 1: Figure S1B). [score:3]
Here, we report that miR-188 is a potent tumor suppressor in human nasopharyngeal carcinoma cells. [score:3]
To create a scenario closer in resemblance to the normal physiological state, we generated CNE cells that stably expressed miR-188 to ascertain its effect on cell proliferation. [score:3]
from qRT-PCR showed that overexpression of miR-188 resulted in 30-50% reduction in transcript abundance for CCND1, CCNA2, CCND3, CCNE1, CDK2 and CDK4 (Figure  2B). [score:3]
By quantifying the level of miR-188 in CNE cells, we found that the expression of miR-188 increased by nearly 1000 folds after transient transfection of miRNA mimics, which is far beyond the level of endogenous miR-188 (Additional file 1: Figure S1A). [score:3]
We found that miR-188 suppressed CDK -mediated Rb phosphorylation since silencing endogenous miR-188 with ant-188 increased the amount of Rb phosophorylation while miR-188 transfected cells showed less Rb phosphorylation (Figure  3E and F, Additional file 4: Figure S3B). [score:3]
Using a pE2F-TA-Luc plasmid that contains four copies of E2F binding elements, we showed that enforced expression of miR-188 remarkably decreased E2F transcriptional activity, as determined by reduced luciferase activity (Figure  3G). [score:3]
The potential miR-188 binding sequences within the 3′UTRs of target genes were predicted by FindTar (Figure  4). [score:3]
MiR-188 directly binds to the 3′UTRs of target genes. [score:3]
We then investigated the expression of miR-188 targets in tumor tissues using western blot. [score:3]
Similar to transiently transfected cells, cell proliferation rate was significantly reduced in the miR-188 stably expressed clones (Figure  1F). [score:3]
Inverse correlation of miR-188 and its target genes in NPC tissues. [score:3]
Strikingly, we observed that overexpression of miR-188 attenuated cell proliferation in CNE cells (Figure  1A and B). [score:3]
Our study provides strong evidence supporting miR-188 may function as a tumor suppressor and it is a potential candidate for anti-cancer therapy. [score:3]
To validate, we overexpressed miR-188 in CNE cells, then harvested cells for mRNA and protein expression level measurements for these six genes. [score:3]
MiR-188 mimics and miRNA inhibitors were synthesized and purified by GenePharma Co. [score:3]
In contrast, the reporter vectors carrying seed mutated 3′UTR fragments abrogated the inhibitory effect of miR-188 on luciferase activity (Figure  4). [score:3]
We found that 2214 genes contain potential miR-188 target sites. [score:3]
Further study from xenograft mouse mo del shows that miR-188 has anti-cancer potential through suppressing tumor initiation and progression. [score:3]
Figure 2 MiR-188 downregulates multiple genes related to G [1] /S transition. [score:3]
Our data indicate that miR-188 expressed cells have slower growth and cell proliferate rate. [score:3]
Similarly, Rb phosphorylation at S811 and S780 residues were significantly reduced in CNE cells stably expressing miR-188 (Additional file 4: Figure S3C, D). [score:3]
Similar results were obtained from miR-188 stably overexpressed cells (Additional file 4: Figure S3A). [score:3]
Together, these results demonstrate that miR-188 suppresses cell proliferation mainly by interrupting G [1]/S cell cycle progression. [score:3]
Approximately 5 × 10 [5] viable CNE cells stably expressing miR-NC or miR-188 were injected subcutaneously into the dorsal flank of nude mice. [score:3]
Having identified the potential targets of miR-188, we then wanted to determine the role of miR-188 on cell cycle progression, especially on G [1]/S transition. [score:3]
Although, there was no significant difference among the colonies between each plate, the colony size of cells stably expressed miR-188 was much smaller than that of the control (Figure  1E). [score:3]
Moreover, miR-188 is capable of inhibiting tumor initiation and progression in xenograft mouse mo del, indicating that miR-188 may have anti-cancer potential in human nasopharyngeal cancer. [score:3]
In order to determine the anti-cancer potential of miR-188 in vivo, nude mice were injected with CNE cells that stably expressed miR-188 or miR-NC. [score:3]
The 3′UTR fragments of target genes containing wild-type (WT) or seed region mutated (Mu) of miR-188 binding sites were inserted into a dual-luciferase reporter vector. [score:3]
A series of cell cycle related genes were potential targets of miR-188. [score:3]
According to pathway annotation summary, the KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway was classified as containing most of the genes identified by DAVID as potential targets of miR-188 (Figure  1G left panel). [score:3]
Using miRNA target prediction algorithms Findtar, we found that six G [1]/S related genes, including CCND1, CCND3, CDK4, CCNA2, CDK2 and CCNE1 contain miR-188 response elements in their 3′UTRs (Figure  2A). [score:3]
The expression of miR-188 in CNE cells. [score:3]
Figure 1 MiR-188 inhibits cell proliferation and tumor colony formation. [score:2]
MiR-188 suppresses Rb phosphorylation and E2F transcriptional activity. [score:2]
Figure 5 MiR-188 suppresses tumor initiation and progression in vivo. [score:2]
MiR-188 also suppresses Rb phosphorylation and E2F transcriptional activity. [score:2]
Figure 6 MiR-188 targets multiple genes involved in G [1] /S cell cycle transition. [score:2]
Compared to control antisense oligonucleotides (ant-NC), the amounts of CCND1, CCNA2, CCND3, CCNE1, CDK2 and CDK4 proteins increased slightly when endogenous miR-188 expression was silenced (Figure  2D, Additional file 3: Figure S2C). [score:2]
To determine whether miR-188 indeed target CCND1, CCND3, CCNA2, CCNE1, CDK2 and CDK4, we employed luciferase reporter assay. [score:2]
However, little is known about the function of miR-188 on cell proliferation and cell cycle regulation. [score:2]
MiR-188 targets multiple cyclin/CDKs involved in G1/S transition. [score:2]
MiR-188 (n = 12) suppressed tumorigenesis compared with miR-NC (n = 10). [score:2]
MiR-188 suppresses tumor formation and progression in nude mice. [score:2]
However, little is known about the function of miR-188 in cell proliferation and growth control. [score:1]
MiR-NC or miR-188 stable cells were plated at 4 × 10 [3] cells per well in 6-well plate. [score:1]
MiR-188, a miRNA located on the X chromosome in humans, was first identified in 2003 [34]. [score:1]
Equal amounts of miR-NC or miR-188 stable cell lines were cultured for 4 days, cell proliferation was monitored at indicated time points. [score:1]
Figure 3 MiR-188 arrests cell cycle at G [1] /S transition through negative regulation of Rb-E2F axis. [score:1]
For synchronization, cells transfected with miR-NC or miR-188 were treated with 2 mM hydroxyurea (Sigma-Aldrich, H8627) for 16 h to block cell at G1 phase. [score:1]
Strikingly, tumor induction was dramatically prevented in miR-188 injected mice (Figure  5A). [score:1]
The protein levels of Cyclin E1, Cyclin D3, Cyclin D1,Cyclin A2, CDK2 and CDK4 were significantly decreased in tumor tissues harvested from miR-188 injected mice (Figure  5D and E). [score:1]
Our data demonstrate a novel mechanism of miR-188 control on cell proliferation and cell cycle progression. [score:1]
The G [1] cell population was bigger in miR-188 transfected CNE cells (21.7 ± 1.38%) than that in control cells (14.6 ± 0.95%) (Figure  3A). [score:1]
There was a significant reduction of BrdU incorporation in miR-188 transfected cells (Figure  3B). [score:1]
The KEGG contains 26 signaling pathways, among these, MAPK signaling pathway (p value: 1.08 × 10 [−5]), ErbB signaling pathway (p value: 3.57 × 10 [−4]), axon guidance (p value: 5.16 × 10 [−3]) and cell cycle (p value: 7.20 × 10 [−3]) were the four pathways most significantly associated with miR-188 according to p values (Figure  1G middle panel, Additional file 2: Table S1). [score:1]
miR-NC (mean: 327.9 mg; range: 39.6 to 659.4 mg); miR-188 (mean: 83.2 mg; range: 19.5 to 136.6 mg). [score:1]
Tumor mass and tumor volume were also significantly lower in mice injected with miR-188 (Figure  5B and C). [score:1]
Sequences of miR-188 and predicted miR-188 -binding sites at CCNA2, CCND1, CCND3, CCNE1, CDK2 and CDK4 3′UTRs. [score:1]
Plasmid carrying GFP and miR-188 hairpin was purchased from GenePharma Co. [score:1]
CNE cells transfected with miR-188 or miR-NC were synchronized at G [1]/S boundary by treatment with hydroxyurea. [score:1]
CNE cells were transfected with miR-188 or miR-NC for 72 h, the representative phase contrast images were shown. [score:1]
Equal amounts of CNE cells were transfected with miR-188 or miR-NC, cell proliferation was monitored at indicated time points. [score:1]
CNE cells were plated at a concentration of 3 × 10 [3] cells per well in 6-well plate and transfected with miR-188 or miR-NC every three day after cells adhesion. [score:1]
The relative levels of miR-188, CCND1, CCND3, CDK4, CCNA2, CDK2 and CCNE1 were quantified using qRT-PCR. [score:1]
These results indicate that miR-188 also plays an important role on Rb phosphorylation. [score:1]
The incorporation of EdU in miR-188 transfected cells was significantly less than that of control cells (Figure  3C and D). [score:1]
CNE cells were transiently transfected with miR-188 plasmid, followed by Blasticidin S (YEASEN, 60218ES10) selection at final concentration of 20 ug/ml. [score:1]
The reporter vectors were co -transfected with miR-188 or miR-NC. [score:1]
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2
[+] score: 237
Other miRNAs from this paper: hsa-mir-224, hsa-mir-149, hsa-mir-193a
Gleason grades of PCa patients with high miR-188-5p expression and miR-188-5p -high/UBE2I-low expression were significantly higher than those of patients with low miR-188-5p expression and miR-188-5p-low/UBE2I -high expression, respectively (both P < 0.05). [score:9]
In PCa tissues, the increased expression of miR-188-5p may negatively regulate the expression of its candidate target gene, UBE2I, which may reduce the degradation of TP73. [score:8]
Wang L Liu H microRNA-188 is downregulated in oral squamous cell carcinoma and inhibits proliferation and invasion by targeting SIX1Tumour Biol. [score:8]
e–h Knockdown of miR-188-5p expression by the corresponding inhibitor efficiently weakened the cellular proliferation, invasion ability and motility of LNCaP cell lines and inhibited the growth of tumor xenografts, but it enhanced cellular apoptosis qin vitro. [score:8]
Fig. 2Overall survival (a–f), biochemical recurrence (BCR)-free survival (g–l) and distant-metastasis-free survival (m–r) curves based on miR-193a and/or TP73 as well as miR-188 and/or UBE2I expression in patients with prostate cancer based on TCGA data The results shown in Supplementary Figure  S4A indicated that the endogenous expression of TP73 in PCa cells and in established tumors associated with LNCaP cells stably expressing miR-193a-5p was significantly reduced at both the mRNA and protein levels. [score:7]
To verify whether TP73 was a direct target of miR-193a-5p, and UBE2I was a direct target of miR-188-5p, a luciferase reporter containing the complimentary seed sequences of miR-193a-5p/miR-188-5p at the 3′-UTR region of TP73 (Transcript NM_001126242, protein name: deltaNp73 gamma) /UBE2I (Transcript NM_003345) mRNA was constructed. [score:7]
In contrast, miR-188-5p overexpression markedly increased the protein expression levels of CCND1 and MDM2 but decreased the protein expression levels of UBE2I, RNASEL and CDKN1A (all P < 0.05). [score:7]
Moreover, the enforced expression of UBE2I in two PCa cell lines markedly reduced the protein expression levels of CCND1 and MDM2 but increased the protein expression levels of RNASEL and CDKN1A (all P < 0.05, Fig.   7d), which were also opposite to the miR-188-5p enforced cells as mentioned above. [score:7]
In this study, we constructed an miRNA -mediated gene expression regulatory network of PCa and identified a novel miRNA–mRNA regulatory biomodule of miR-193a-5p- and miR-188-5p-regulated CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I signaling. [score:6]
Interestingly, knockdown of miR-188-5p expression by the corresponding inhibitor reduced the enhanced effects on cellular proliferation, invasion and motility of PCa cell lines and the growth of tumor xenografts, but it increased cellular apoptosis in vitro (Fig.   5f–j and Supplementary Figure  S9E–H). [score:6]
Additionally, UBE2I was a putative target of miR-188-5p (PCa -upregulated miRNA, Supplementary Table  S1) and interacted with TP73 and CDKN1A through MDM2 (Fig.   1a). [score:6]
In addition, PCa patients with high miR-188-5p or low UEB2I expression had a higher incidence of biochemical recurrence than those with low miR-188-5p or high UBE2I expression (both P < 0.05). [score:5]
Both low UBE2I expression and combined miR-188-5p -high/UBE2I-low expression were significantly associated with advanced T stage (both P < 0.05). [score:5]
These experiments were performed after co-transfection of miR-188-5p mimics and/or the UBE2I 3′-UTR (−) for 48 h. The data are representative of at least three independent experiments and are presented as the mean ± s. e. m. Note: ‘×10’ and ‘×20’ refer to the magnification These findings suggest that the onco-miRNA roles of miR-188-5p may be mediated by inhibiting its target gene, UBE2I. [score:5]
PCa patients with miR-188-5p -high/UBE2I-low expression frequently experienced advanced N stage and recurred/progressed disease status (both P < 0.05, Table  1). [score:5]
These experiments were performed after co-transfection of miR-188-5p mimics and/or the UBE2I 3′-UTR (−) for 48 h. The data are representative of at least three independent experiments and are presented as the mean ± s. e. m. Note: ‘×10’ and ‘×20’ refer to the magnification These findings suggest that the onco-miRNA roles of miR-188-5p may be mediated by inhibiting its target gene, UBE2I. [score:5]
Fang F MicroRNA-188-5p suppresses tumor cell proliferation and metastasis by directly targeting FGF5 in hepatocellular carcinomaJ. [score:5]
Our data showed that miR-193a-5p and miR-188-5p targeted TP73 and UBE2I respectively at mRNA and protein level, suggesting that the two miRNAs may not work at the translational level throughout a DICER mechanism. [score:5]
Collectively, this integrated analysis of an miRNA -mediated gene expression regulatory network reveals the potential roles of miR-193a-5p/TP73 and miR-188-5p/UBE2i negative regulation pairs in PCa. [score:5]
Note: ‘×10’ and ‘×20’ refer to the magnification a Endogenous UBE2I protein expression levels were detected by western blotting in LNCaP cells transfected with the miR-188-5p mimic in the presence of UBE2I or vector control for 48 h. b–e Expression of UBE2I using a construct lacking its 3′-UTR rescued the biological effects associated with re-introduction of miR-188-5p, as indicated by cell invasion, viability, migration and apoptosis assays. [score:4]
The above data suggest that TP73 and UBE2I may be direct targets of miR-193a-5p and miR-188-5p, respectively, in PCa cells. [score:4]
Fig. 6 a Endogenous UBE2I protein expression levels were detected by western blotting in LNCaP cells transfected with the miR-188-5p mimic in the presence of UBE2I or vector control for 48 h. b–e Expression of UBE2I using a construct lacking its 3′-UTR rescued the biological effects associated with re-introduction of miR-188-5p, as indicated by cell invasion, viability, migration and apoptosis assays. [score:4]
b Molecular mo del of the miR-193a-5p and miR-188-5p-regulated CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I signal axis in PCa cellsCyclin D1 (CCND1) is amplified and overexpressed in a variety of human malignancies, including human PCa 11, 12. [score:4]
b Molecular mo del of the miR-193a-5p and miR-188-5p-regulated CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I signal axis in PCa cells Cyclin D1 (CCND1) is amplified and overexpressed in a variety of human malignancies, including human PCa 11, 12. [score:4]
TP73 and UBE2I are respective direct targets of miR-193a-5p and miR-188-5p in PCa cells. [score:4]
In contrast, the apoptotic rates of LNCaP and PC3 cells with miR-188-5p upregulation were significantly lower than those of control cells (Fig.   5e and Supplementary Figure  S9D). [score:4]
d The apoptotic rate of LNCaP cells with miR-188-5p upregulation was significantly lower than that of control cells. [score:4]
Note: ‘×10’ and ‘×20’ refer to the magnificationIn the rescue experiments, the endogenous expression of UBE2I protein in LNCaP and PC3 cells transfected with miR-188-5p mimics in the presence of pCDNA3.1-UBE2I was significantly higher than that in cells transfected with miR-188-5p and vector control (Fig.   6a and Supplementary Figure  S10A). [score:3]
Re -expression of UBE2I rescues the oncogenic effects of miR-188-5p in LNCaP cells. [score:3]
In contrast, Zhang’s miRNA array data displaying the decreased expression of miR-188-5p were obtained from paired metastatic LTL-313H and non-metastatic LTL-313B PCa xenografts. [score:3]
We illustrated a mo del to hypothesize the involvement of the miR-193a-5p-regulated and miR-188-5p-regulated CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I signal axis in prostate carcinogenesis (Fig.   1b). [score:3]
In addition to the significant clinical relevance, miR-193a-5p- and miR-188-5p-regulated CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I signaling may be a novel regulatory biomodule within prostate carcinogenesis. [score:3]
Using this larger data set, we demonstrated that high-miR-188-5p and/or low-UBE2I expression was significantly associated with aggressive PCa progression and poor patient prognosis. [score:3]
There were no significant prognostic values of miR-193a-5p/TP73 and miR-188-5p/UBE2I axes in overall and disease metastasis-free survivals (Fig.   2a–f and Fig.   2m–r). [score:3]
miR-188-5p promotes LNCaP cell proliferation, migration and invasion and in vivo tumor growth, but it suppresses LNCaP cell apoptosis. [score:3]
Note: ‘×10’ and ‘×20’ refer to the magnification In the rescue experiments, the endogenous expression of UBE2I protein in LNCaP and PC3 cells transfected with miR-188-5p mimics in the presence of pCDNA3.1-UBE2I was significantly higher than that in cells transfected with miR-188-5p and vector control (Fig.   6a and Supplementary Figure  S10A). [score:3]
: miR01101-1-5), miR-188-5p inhibitor (anti-miR-188, Cat. [score:3]
Moreover, only miR-188-5p -high/UBE2I-low expression was significantly associated with short BCR-free survival (P = 0.045, log-rank test, Fig.   2l). [score:3]
b Relative protein expression levels of UBE2I, CCND1, RNASEL, CDKN1A, and MDM2 in LNCaP and PC3 cells transfected with miR-188/NC -mimics. [score:3]
First, the microarray data showing the marked upregulation of miR-188-5p in PCa tissues compared with adjacent non-cancerous prostate tissues were based on clinical samples. [score:3]
Notably, Zhang et al. [28] suggested that miR-188-5p might exert tumor suppressor functions in the carcinogenesis of PCa, which disagrees with our findings. [score:3]
miR-188-5p functions as an onco-miRNA in PCa by targeting UBE2I. [score:3]
miR-188, a cancer-related miRNA, functions as a tumor suppressor in oral squamous cell carcinoma [26] and hepatocellular carcinoma [27]. [score:3]
In vitro cellular proliferation (Fig.   6b and Supplementary Figure  S10B), invasion (Fig.   6c and Supplementary Figure  S10C), migration (Fig.   6d and Supplementary Figure  S10D), and apoptosis (Fig.   6e and Supplementary Figure  S10E) all indicated that restoration of UBE2I expression dramatically attenuated the effects induced by miR-188-5p. [score:3]
To evaluate the associations of miR-193a-5p-TP73 and miR-188-5p-UBE2I expression with various clinicopathological features of PCa patients, the optimal cutoff points of miR-193a-5p, TP73, miR-188-5p and UBE2I expression were screened. [score:3]
Based on the in vivo system, miR-188-5p overexpression promoted tumor growth (Fig.   5d). [score:3]
Our experimental validations further confirmed the regulatory effects of miR-193a-5p and miR-188-5p on this signaling axis at both mRNA and protein levels. [score:2]
b Molecular mo del of the miR-193a-5p and miR-188-5p-regulated CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I signal axis in PCa cells a Sub-network of the CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I signal axis and the corresponding upstream microRNAs. [score:2]
After validation of the clinical significance and the biological functions of the miR-193a-5p-TP73 and miR-188-5p-UBE2I axes, we investigated their regulatory effects on the protein expression levels of CCND1, RNASEL, CDKN1A, and MDM2 by western blot analysis. [score:2]
Transwell and wound-healing assays showed that the enforced expression of miR-188-5p dramatically enhanced the invasive and migratory activities, respectively, of both LNCaP and PC3 cells (Figure  5b, c and Supplementary Figure  S9B, C). [score:2]
Involvement of the miR-193a-5p and miR-188-5p-regulated CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I signal axis in prostate cancer (PCa) cells. [score:2]
c The wound-healing assay revealed that miR-188-5p overexpression efficiently enhanced the migratory ability of LNCaP cells. [score:2]
Deregulation of miR-193a-5p-TP73 and miR-188-5p-UBE2I pairs associated with aggressive progression and poor prognosis in PCa patients. [score:2]
These experiments were performed after co-transfection of miR-188-5p mimics and/or the UBE2I 3′-UTR (−) for 48 h. The data are representative of at least three independent experiments and are presented as the mean ± s. e. m. Note: ‘×10’ and ‘×20’ refer to the magnification According to our above-mentioned network analysis, the CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I axis may play crucial roles in the imbalanced miRNA -mediated regulatory network of human PCa. [score:2]
Based on the molecular interactions and the implications of this signaling in cancer 11– 20, 30, we illustrated a biomodule of miR-193a-5p- and miR-188-5p-regulated CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I signaling in Fig.   1b. [score:2]
Taken together, an imbalance of the miR-193a-5p- and miR-188-5p-regulated CCND1 -RNASEL-CDKN1A-TP73-MDM2-UBE2I biomodule might be involved in prostate carcinogenesis. [score:2]
These findings suggest that CCND1, RNASEL, CDKN1A, and MDM2 may function as the downstream effectors of the miR-193a-5p-TP73 and miR-188-5p-UBE2I axes. [score:1]
We also determined the downstream effectors of the miR-193a-5p/TP73 and miR-188-5p/UBE2i axes. [score:1]
Commercial miR-188-5p mimics (miR-188 -mimic, Cat. [score:1]
b The transwell assay showed that the enforced expression of miR-188-5p significantly enhanced the invasive activities of LNCaP cells compared with those of control cells. [score:1]
The findings for the miR-188-5p/UBE2I pair were similar to those for the miR-193a-5p/TP73 pair (Supplementary Figure  S4B). [score:1]
These findings were similar with those for the miR-188-5p/UBE2I pair (Supplementary Figure  S6B). [score:1]
CCND1, RNASEL, CDKN1A, and MDM2 function as the downstream effectors of the miR-193a-5p-TP73 and miR-188-5p-UBE2I axes. [score:1]
Using the optimal cutoff points, 490 PCa patients were divided into miR-193a-5p -high/low, TP73 -high/low, miR-188-5p -high/low and UBE2I -high/low groups. [score:1]
Western blot analysis indicated that CCND1, RNASEL, CDKN1A and MDM2 function as the downstream effectors of the miR-193a-TP73 and miR-188-UBE2I axes at a protein level. [score:1]
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3
[+] score: 115
Other miRNAs from this paper: hsa-mir-31, oar-mir-3957
In the present study, we demonstrated that miR-188 directly target DLX3 and SNP4 affects miR-188 -mediated regulation of DLX3 gene expression. [score:7]
Taken together, all these results demonstrated that miR-188, not miR-3957-5p, directly targets DLX3, and SNP4 affects miR-188 -mediated downregulation of DLX3. [score:7]
To further validate whether miR-188 targets sheep DLX3 3'UTR and whether SNP4 affects miR-188 -mediated regulation of DLX3 gene, we tested the effect of miR-188 on DLX3 3'UTR reporter activity using miRNA synthetic inhibitors, a class of chemically engineered oligonucleotides that prevent endogenous miRNA. [score:6]
MiR-31 and miR-188 downregulate the gene expression of DLX3, HOXC13, GATA3, KRT71 and LEF1 mRNA in SFFs. [score:6]
We first performed miRNA and gene expression analysis in sheep skin and SFFs, and the results showed that miR-188, miR-3957-5p, miR-31 and DLX3 were to some extent expressed in both sheep skin and SFFs (Fig 2A), implying that it is possible that miR-188 and miR-3957-5p regulate sheep DLX3 gene posttranscriptionally. [score:6]
Our results showed that sheep DLX3 is a target of miR-188, and the SNP4 in 3′UTR of sheep DLX3 affects miR-188 -mediated downregulation of DLX3 (S2A Fig), possibly contributing to the wool trait variation in our tested population. [score:6]
To further test whether miR-188 and miR-3957-5p directly regulate DLX3 expression and whether SNP4 and SNP3 affect miRNA regulation of sheep DLX3, we performed luciferase reporter assays in both SFFs and HaCaT cells using miRNA mimics. [score:5]
These expression data suggest that miR-188 may be a new important regulator in hair follicle development and hair formation. [score:5]
First, we checked whether miR-188 inhibitor could reduce endogenous miR-188 expression. [score:5]
However, we just provided evidence that the SNP4 affects DLX3 gene regulation, at least in part, by interfering with miR-188 -mediated downregulation of DLX3 gene. [score:5]
The real-time RT-PCR expression analysis showed that, similar to miR-31, in agreement with reporter gene findings, miR-188 mimc reduced the endogenous DLX3 gene expression in SFFs, compared to the mimics negative control (S2A Fig), which is in agreement with reporter gene findings. [score:4]
Taken together, these data suggest miR-188 may regulate sheep DLX3 and SNP4 affects DLX3 gene expression. [score:4]
The result showed that miR-188 inhibitor (anti-miR-188) indeed could significantly reduce miR-188 expression in SFFs compared to the control (S1B Fig). [score:4]
The results showed that, similar to miR-31, miR-188 regulated the expression of these genes (HOXC13, GATA3, KRT71 and LEF1) in SFFs (S2B–S2E Fig). [score:4]
Second, the reporter gene assays showed that in SFFs (mesenchymal cells) and HaCaT cells (epidermal cells), miR-188 mimic decreased its allele D reporter (psiCHECK2-TCAD) activity (Fig 2C and 2D), and miR-188 inhibitor increased its allele D reporter activity (Fig 3A and 3C), and neither miR-188 mimic nor miR-188 inhibitor had significant effect on its allele I reporter activity (Figs 2E, 3B and 3D). [score:4]
0137135.g003 Fig 3(A, B) Effect of miR-188 inhibitor on reporter activity of psiCHECK2-TCAD and TCAI in SFFs. [score:3]
In addition, miR-188 decreased the endogenous expression of hair follicle–associated genes HOXC13, GATA3, keratin 71 (KRT71) and lymphoid enhancer binding factor 1 (LEF1) (S2B–S2E Fig). [score:3]
The evidence is as follows: First, here is a putative miR-188 binding site in the 3′UTR of sheep DLX3, and miR-188 and DLX3 were coexpressed in sheep skin and SFFs. [score:3]
In summary, our findings for the first time demonstrate that DLX3 is a target of miR-188, and the SNP c. *1,038_1,039 insC affects miR-188 -mediated downreguation of sheep DLX3 gene, possibly contributing to wool phenotypic variation. [score:3]
Among the list of predicted miRNAs (S1 Table), only miR-188 is well known for its expression and involvement in hair follicle [19, 20]. [score:3]
Finally, miR-188 decreased the endogenous DLX3 mRNA expression in SFFs. [score:3]
Effect of miR-188 inhibitor on the reporter activity of psiCHECK2-TCAD and psiCHECK2-TCAI reporters. [score:3]
Here, we detected the effect of miR-188 on the endogenous expression of DLX3 and other several hair follicle -associated genes. [score:3]
The following primers were used for miRNA expression analysis: miR-31: 5′-CAGGCAAGATGCTGGCATAGCT-3′; miR-188: 5′-ATCCCTTGCATGGTGGAGGGT-3′. [score:2]
Therefore, in the subsequent study, we tested whether these two SNPs (SNP3 and SNP4) affect miRNA regulation of sheep DLX3 by miR-3957-5p and miR-188. [score:2]
In the present study, we demonstrated that the SNP4 (c. *1,038_1,039 insC) affects miR-188 -mediated regulation of DLX3, possibly contributing to the wool crimp variation. [score:2]
Effects of miR-188 on DLX3 3'UTR Luciferase Reporter activity. [score:1]
Finally, we investigated the effect of miR-188 mimic on endogenous expression of DLX3 and some other hair follicle–associated genes in SFFs. [score:1]
SNP3 and SNP4 were predicted to be located within the putative binding sites of miR-3957-5p and miR-188, respectively, in the 3′UTR of sheep DLX3 mRNA. [score:1]
MiR-188 inhibitor increased reporter activity of psiCHECK2-TCAD (C), not psiCHECK2-TCAI (D) in HaCaT cells, compared to the negative control. [score:1]
However, anti-miR-188 had no clear effect on reporter activity of psiCHECK2-TCA I (allele I) reporter in both SFFs and HaCaT cells (Fig 3B and 3D). [score:1]
Then we tested the effect of anti-miR-188 on the reporter activity of two individual haplotype reporters (psiCHECK2-TCA D and psiCHECK2-TCA I). [score:1]
MiR-188 inhibitor increased the luciferase activity of psiCHECK2-TCAD (A), not psiCHECK2-TCAI (B) in SFFs, compared to the negative control. [score:1]
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4
[+] score: 45
The analysis of the prognostic value of dysregulated miRNAs show that higher relative expression of miR-21 and miR-188 is associated with worse outcome in our cohort of resectable NSCLC. [score:4]
In contrast, the expression levels of miR-188 were very low in normal and even in tumor samples. [score:3]
MiR-21 or miR-188 overexpression correlated with a negative prognosis, and their combined signature may represent a new independent prognostic biomarker for RFS and OS. [score:3]
In addition, functional analyses were performed with the prognostic value miRNAs (miR-21 and miR-188), where target gene enrichments were carry out. [score:3]
Survival analyses showed that miR-21-5p or miR-188-5p overexpression were negative prognostic factors, implicating miR-188 in NSCLC for the first time. [score:3]
Of the 22 miRNAs analyzed, only miR-21-5p and miR-188-5p had any prognostic value: higher expression of these miRNAs was significantly correlated with shorter RFS (24.03 vs. [score:3]
Finally, we identified a patient subgroup defined by a combined higher expression levels of miR-21 and miR-188 that exhibited poor outcome and resulted in an independent prognostic factor for RFS (HR: 0.485 [0.313-0.753]; p = 0.001) and OS (HR 0.389 [0.237-0.638]; p < 0.0001) in multivariate analysis, suggesting its potential role as biomarker useful for distinguishing patients which could benefit from more exhaustive monitoring. [score:3]
In concordance with our results, in patients with acute myeloid leukemia (cytogenetically-normal), high miR-188 expression has been significantly associated with shorter OS and event-free survival [89]. [score:3]
Interestingly, the group of patients with high expression of both miRNAs (miR-21 [high] and miR-188 [high]) showed shorter relapse-free survival (RFS) and overall survival (OS) times. [score:3]
Our results obtained in the validation set by also indicated that patients with elevated miR-188 expression in tumor tissue had a shorter RFS (p = 0.009) and OS (p = 0.002). [score:3]
Interestingly, patients with high expression of both miRNAs (miR-21 [high] and miR-188 [high]) had shorter RFS and OS times (p = 0.006 and p = 0.0006, respectively) (Table 4, Figure 2C). [score:3]
Analysis revealed a poor prognosis for OS in patients with high levels of miR-21 (37.86 vs 59.66 months, p = 0.020) (Figure 2D); however miR-188 did not show prognostic value in the group of TCGA patients. [score:1]
Figure 2Panels A and B show OS and RFS for miR-21-5p and miR-188-5p, respectively in the validation set. [score:1]
Although the computational analysis has shown a relationship of miR-188 with the carcinogenesis process, further studies are still needed to clarify the function of this miRNA in carcinogenesis and its prognostic implication in cancer. [score:1]
Panels A and B show OS and RFS for miR-21-5p and miR-188-5p, respectively in the validation set. [score:1]
This can explain why miR-188 cannot find a prognosis value in TCGA cohort. [score:1]
org/releases/current/projects/LUSC-US MiR-21-5p and miR-188-5p RPKM values were extracted using their genomic positions, obtained from miRBase. [score:1]
82.60 0.043 -- -- -- -- -- -- miR-188-5p (high vs. [score:1]
KRAS status was an independent prognostic variable for RFS according to the Cox regression mo del (p = 0.020) and the signature (miR-21 [high] and miR-188 [high]) was an independent poor prognostic biomarker for RFS (p = 0.001) and OS (p < 0.0001) (Table 4). [score:1]
There are limited studies analyzing the prognostic role of miR-188 in cancer [89– 91], and in fact none has been found in lung cancer to date. [score:1]
Clinicopathological characteristics of these patients are summarized in Table 1. The analyses confirmed that both miR-21 and miR-188 were significantly overexpressed in tumor tissues (p < 0.0001). [score:1]
NR 0.002 -- -- -- -- -- -- Combined miRNAs (miR-21 [high] miR-188 [high] vs. [score:1]
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5
[+] score: 22
Mutation of miR-9 binding site did not change the activity of the reporter in miR-9 transfected cells while mutation of the miR-188 binding site slightly increased the susceptibility of the reporter to the inhibition by the miR mimic. [score:5]
miR-133a, miR-138, miR-188, miR-342, miR-491, and miR-541 were co -transfected into HeLa cells with a reporter plasmid containing the appropriate 3′UTR and their ability to inhibit reporter activity was analyzed as described for the hTERT 3′UTR. [score:3]
The miR-9, and miR-188 had no significant inhibitory effect on the WT reporter activity relative to the scrambled miR control. [score:3]
The experiments above demonstrated that the transfection of the miRNAs (miR-138, miR-188, miR-342, miR-491, miR-541) inhibit TCF7 and MSI1 3′UTR reporters, therefore, we analyzed their ability to alter the endogenous protein levels of these genes in DLD-1 cells (Figure 5). [score:3]
This gene was shown previously to be regulated by miR-138 [55] and our results demonstrated that it is also under regulation of miR-188, miR-342, miR-491, and miR-541. [score:3]
In order to determine whether miRNAs may also cooperate to inhibit cell proliferation, DLD-1 and MCF-7 cell lines were treated with three combinations of miRNAs as described in Figure 3 with the difference that miR-188 was also a part of MIX1 and MIX3 (Figure 6b). [score:3]
We selected four miRNAs (miR-188-3p, 342-5p, 491-5p, and 541-3p), which have binding sites in the 3′UTR of three other genes, TCF7, MSI1, and PAX5 (Figure 1b). [score:1]
The other two genes, MSI1 and PAX5, share binding sites for five different miRNAs, including multiple sites for miR-188-3p, 342-5p, 491-5p and 541-3p (twelve in MSI1 and eight in PAX5 3′UTRs) with the 3′UTR of hTERT. [score:1]
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6
[+] score: 19
Other miRNAs from this paper: hsa-mir-765
Among them, mir-188 and mir-765 present the most of new predictions with diseases, and could be ubiquitous biomarkers of some diseases. [score:5]
Mir-188 dysregulation is reported in various diseases such as Alzheimer’s disease 50, 51, azoospermia [52], breast cancer [53], some carcinoma 54– 56, leukemia 57, 58, infarction [59], myeloma [60], pre-eclampsia [61] and prostate cancer [62]. [score:5]
mir-188 and mir-765 are predicted to play a role in several diseases. [score:3]
Among the 72 remaining putative associations, most of them imply mir-188 and mir-765 with several diseases (32 and 21 respectively) (Supplementary Table  S6). [score:3]
Mir-188 takes part in the cell cycle maintenance (cell proliferation, G1/S cell cycle transition, tumor colony formation) by targeting genes implied in the cell cycle checkpoints (CCND1, CCND3, CCNE1, CCNA2, CDK4 and CDK2) [63]. [score:2]
Figure 5 Main biological processes and pathways known for mir-188 and mir-765. [score:1]
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7
[+] score: 16
APF directly inhibits miR-188-3p and leads to increased ATG7 expression, which results in increased autophagy and infarct size [65]. [score:6]
Wang et al. revealed that miR-188-3p can suppress autophagy and MI damage through its target on ATG7, an enzyme known to be a key player in the autophagy pathway [82]. [score:5]
Wang K. Liu C. Y. Zhou L. Y. Wang J. X. Wang M. Zhao B. Zhao W. K. Xu S. J. Fan L. H. Zhang X. J. APF lncRNA regulates autophagy and myocardial infarction by targeting miR-188-3p Nat. [score:4]
Furthermore, the lncRNA autophagy-promoting factor (APF) has been shown to modulate autophagic cell death and MI through its interaction with miR-188-3p (Table 2 and Figure 2). [score:1]
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8
[+] score: 14
The ventricular-restricted expression pattern of miR-1, -30b, -126, -133, and -499 starkly contrasted the reverse pattern of pluripotency -associated miRs that were differentially expressed in hESCs, and the stable expression levels of miR-188 and -296, which remained relatively unchanged across the different developmental stages examined as reflected by the small variances (Figure 1A, D). [score:8]
Of note, miR-188 was shown to display the most stable expression profile across all cell types examined. [score:3]
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]
Indeed, the stability of miR-188 and -296 was comparable to the endogenous controls RNU38B and RNU48. [score:1]
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9
[+] score: 12
We found that LMP1 could induce the expression of several miRNAs such as miR-155, miR-188, miR-181b while other cellular miRNAs such as miR-103, miR-107 were downregulated. [score:6]
LMP2A also induced the expression of a variety of cellular miRNAs such as miR-155, miR-188, miR-181b while some other cellular miRNAs such as miR-125b were downregulated (Table 1 ). [score:6]
[1 to 20 of 2 sentences]
10
[+] score: 10
In this study we discovered three key known AMD genes, Fms related tyrosine kinase 1(Flt1), the receptor for vascular endothelial growth factor (VEGF) (putative miR1192 target), ATP binding cassette subfamily A member 1 (Abca1) (putative miR673-5p target), and Activated leukocyte cell adhesion molecule(Alcam) (putative miR188-3p target) are regulated by Nr2e3 and Rora and their potential corresponding miRNAS that are differentially expressed in Nr2e3 rd7/ rd7 retinas. [score:10]
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11
[+] score: 10
Other miRNAs from this paper: hsa-mir-362, hsa-mir-346, hsa-mir-300
confirmed an upregulation of miR-300 in the YFP+ (CPC-B+) population, but not miR-188 or miR-362, which were not overrepresented in the YFP− population (Figure 1f). [score:4]
The expression profile of three miRNAs, miR-300, miR-188, and miR-362, was validated by RT-qPCR, but miR-346 was not confirmed (Figure 1d). [score:3]
The expression profile of the three confirmed miRNAs in CPCs corresponded to miR-362>miR-188>miR-300 (Supplementary Figure S3b). [score:3]
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12
[+] score: 10
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
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13
[+] score: 9
In anoxia/reoxygenation (A/R) -induced autophagy of cardiomyocytes, the lncRNA autophagy promoting factor (APF) is upregulated to protect ATG7 from being downregulated by miR-188-3p, and thereby promotes autophagic death of cardiomyocytes. [score:7]
[106] Intriguingly, despite the poor conservation of full-length APF across species, the binding site for miR-188-3p is highly conserved, highlighting the significance of the APF/miR-188-3p/ ATG7 regulatory axis in autophagy activation. [score:2]
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14
[+] score: 9
A previous study [5] revealed that the level of miR-188 expression is markedly higher in BMSCs from aged compared with young mice and humans, and the BMSC-specific inhibition of miR-188 stimulated new bone formation. [score:4]
Li et al. [5] found that miR-188 was highly expressed in aged mice and humans and that it regulates the bifurcation of differentiating BMSCs into osteoblasts and adipocytes. [score:4]
Previously, we performed miRNA microarray analysis to determine that miR-188 becomes remarkably elevated in BMSCs with age, and we identified its vital function in determining the differentiation potential of BMSCs. [score:1]
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15
[+] score: 9
For example, the lncRNA MALAT1 modulates SR splicing factor phosphorylation [116], whereas miR-188-5p which is complementary to the PD -induced lncRNAs targets the alternative splicing regulatory factor SFRS1 (SF2/ASF) [117] (which we previously reported as modified in PD patients through exon microarray analysis). [score:4]
These included hsa-miR-188-3p which controls dendritic plasticity and synaptic transmission [70], as well as hsa-miR-125b, which promotes neuronal differentiation and inflammation in human cells by repressing multiple targets [71] (Figure 4A, enlarged). [score:3]
Enrichment analysis of miRNA binding sites in transcripts detected as alternatively spliced by exon level SI analysis of leukocytes from PD patients pre-DBS compared to controls detected 364 miRNA-target binding predictions (Table S5B), including the synaptic plasticity human hsa-miR-188 and the inflammation controlling hsa-mir-125. [score:2]
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16
[+] score: 9
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-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, 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-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-198, hsa-mir-199a-1, hsa-mir-148a, 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-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, 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-135a-1, hsa-mir-135a-2, hsa-mir-142, hsa-mir-145, 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-146a, hsa-mir-150, hsa-mir-186, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, 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-362, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-382, hsa-mir-340, hsa-mir-328, hsa-mir-342, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-335, hsa-mir-345, hsa-mir-196b, hsa-mir-424, hsa-mir-425, hsa-mir-20b, hsa-mir-451a, hsa-mir-409, hsa-mir-484, hsa-mir-486-1, hsa-mir-487a, hsa-mir-511, hsa-mir-146b, hsa-mir-496, hsa-mir-181d, hsa-mir-523, hsa-mir-518d, hsa-mir-499a, hsa-mir-501, hsa-mir-532, hsa-mir-487b, hsa-mir-551a, hsa-mir-92b, hsa-mir-572, hsa-mir-580, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-590, hsa-mir-599, hsa-mir-612, hsa-mir-624, hsa-mir-625, hsa-mir-627, hsa-mir-629, hsa-mir-33b, hsa-mir-633, hsa-mir-638, hsa-mir-644a, hsa-mir-650, hsa-mir-548d-1, hsa-mir-449b, hsa-mir-550a-3, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-454, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-708, hsa-mir-216b, hsa-mir-1290, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-3151, hsa-mir-320e, hsa-mir-378c, hsa-mir-550b-1, hsa-mir-550b-2, 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, hsa-mir-486-2
Low miR-188-5p expression was associated with up-regulation of FOSB, small nucleolar family (SNORD50A, SNORD105, SNORD11B) and zinc finger protein in AML patients. [score:6]
Reduced miR-188-5p expression was associated with a favorable prognosis as indicated by longer overall survival and event-free survival in cytogenetically normal AML patients [100]. [score:3]
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17
[+] score: 8
9 −3.8 hsa-miR-424 −4.2 −2 −4.5 hsa-miR-24-1* −3.9 −2.3 −4.1 hsa-miR-542-3p −2.9 −2.2 −3.8 hsa-miR-29b −2.6 −2.1 −3.3 hsa-miR-301a −2.4 −1.8 −2 hsa-miR-107 −2 −1.7 −2.2 hsa-miR-101 −1.8 −1.9 −1.8 hsa-miR-188-5p −1.7 −1.6 −1.8 Based on the 3 lists of DEMs, we focused our attention on the miRNAs whose expression was influenced specifically by the oncogenic alteration of AKT1, PIK3CA or PTEN, and, alternatively, on those commonly deregulated by two or three of the above-mentioned alterations. [score:4]
9 −3.8 hsa-miR-424 −4.2 −2 −4.5 hsa-miR-24-1* −3.9 −2.3 −4.1 hsa-miR-542-3p −2.9 −2.2 −3.8 hsa-miR-29b −2.6 −2.1 −3.3 hsa-miR-301a −2.4 −1.8 −2 hsa-miR-107 −2 −1.7 −2.2 hsa-miR-101 −1.8 −1.9 −1.8 hsa-miR-188-5p −1.7 −1.6 −1.8Based on the 3 lists of DEMs, we focused our attention on the miRNAs whose expression was influenced specifically by the oncogenic alteration of AKT1, PIK3CA or PTEN, and, alternatively, on those commonly deregulated by two or three of the above-mentioned alterations. [score:4]
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18
[+] score: 8
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-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
In the microarray data, 12 miRNAs were consistent in their change either with HHcy or diabetes; of which 4 miRNAs were downregulated in both groups (miR-16, miR-1983, miR-412 and miR-487) and 8 miRNAs (miR-194, miR-188, miR-1896, miR-467e, miR-504, miR-5110, miR-669k and miR-696) were upregulated in both groups. [score:7]
ARPE_cont) Homo sapiens hsa-miR-4454 0.00806874 –2.15149 Homo sapiens hsa-miR-664a-5p 0.00933842 –1.71214 Homo sapiens HBII-316 0.0371439 –1.6763 Homo sapiens hsa-miR-188-3p 0.0050997 –1.67318 Homo sapiens hsa-mir-548al 0.0409855 –1.66795 Homo sapiens hsa-miR-548ap-3p 0.00270826 –1.62928 Homo sapiens hsa-miR-6888-5p 0.0244117 –1.55839 Homo sapiens hsa-miR-584-5p 0.00101538 –1.54123 Homo sapiens hsa-miR-4681 0.0273394 –1.53062 Homo sapiens hsa-miR-451a 0.0147813 –1.52959 Homo sapiens HBI-36 0.0477323 –1.51987 Homo sapiens hsa-miR-6825-5p 0.0137077 –1.51982 Homo sapiens hsa-miR-4790-5p 0.0229827 –1.51921 Homo sapiens hsa-mir-556 0.00579586 –1.5192 Homo sapiens hsa-mir-4804 0.018718 –1.4998 Homo sapiens U73a 0.0395006 –1. [score:1]
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[+] score: 7
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]
Experimental evidence for the existence of nuclear miRNAs was also present for the three miRNA families, namely miR-188, miR-671 and miR-30. [score:1]
Some miRNAs in six families (miR-34, miR-188, miR-671, miR-340, miR-221, miR-1306) were shown by at least one experimental study to be nuclear dominant. [score:1]
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[+] score: 7
In the second group, there were six miRNAs with an expression level that was four times lower in BCSCs than in MCF-7 cells: miR-200a, miR-301, miR-188, miR-21, miR-181d and miR-29b. [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]
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]
Parts of the amplification curves for miR-188, miR-200a miR-301 and miR-31 are shown (B). [score:1]
Part of amplification curves for miR-188, miR-200a miR-301 and miR-31 are shown in Figure 3B. [score:1]
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[+] score: 6
miR-188 13.3Expressed in DRG and upregulated after sciatic nerve resection [47]. [score:6]
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[+] score: 6
In this study, five miRNAs (miR-29a, miR-29b, miR-126*, miR-127-3p, miR324-3p) were found upregulated and four (miR-188-5p, miR-25, miR-320a, miR-346) downregulated in both quiescent and active UC compared to healthy controls (Fasseu et al., 2010). [score:6]
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[+] score: 6
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-17, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-30a, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-105-1, hsa-mir-105-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-205, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-141, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-320a, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-302a, hsa-mir-34c, hsa-mir-30e, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-372, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-383, hsa-mir-339, hsa-mir-133b, hsa-mir-345, hsa-mir-425, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-193b, hsa-mir-181d, hsa-mir-498, hsa-mir-518f, hsa-mir-518b, hsa-mir-520c, hsa-mir-518c, hsa-mir-518e, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-503, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-376a-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-645, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-744, 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-302e, hsa-mir-302f, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-320e, hsa-mir-548x, hsa-mir-378c, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, 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-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-371b, 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-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
An antisense construct inhibiting miR-15a increased PCNA, while an antisense construct of miR-188 did not affect PCNA expression. [score:5]
In the next step, two selected antisense constructs blocking the corresponding miRNAs miR-15a and miR-188 were used to evaluate their effects on the expression of PCNA. [score:1]
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[+] score: 6
Other miRNAs from this paper: hsa-mir-155, hsa-mir-769
Of all the predicted targets that correlated with the corresponding gene on the transcript level (S2 File and Fig 4A, Panel II), two of the LAPTM4B/miR-188 genes were especially interesting: PVR (Poliovirus receptor protein), and SNX22 (Sorting nexin-22). [score:3]
Thus, our data suggest that the mRNA levels of these genes are regulated by miRNA-188, together with LAPTM4B mRNA. [score:2]
For three of the genes of interest, we identified experimentally validated miRNAs relevant in the context of breast cancer: for ERBB2, miR-155 [36], for LAPTM4B, miR-188 [37], and for NDRG1, miR-769 [38]. [score:1]
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[+] score: 6
miR-532-5p (Figure  2B; mean fold change 2.4), miR-188-3p (Figure  2C; mean fold change 2.5), miR-362-5p (Figure  2D; mean fold change 4.0), miR-501-3p (Figure  2E; mean fold change 5.3), miR-660-3p (Figure  2F; mean fold change 2.2), and miR-502-5p (Figure  2G; mean fold change 3.0) were all markedly up-regulated in the triple -negative breast cancers compared to the normal breast tissue controls. [score:3]
Relative expression levels of (B) miR-532-5p, (C) miR-188-3p, (D) miR-362-5p, (E) miR-501-3p, (F) miR-660-3p, and (G) miR-502-5p in triple -negative breast cancer tissues (n = 19) and adjacent normal tissues (n = 4) are shown. [score:3]
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[+] score: 6
Seven miRNAs (mmu-miR-574-5p, mmu-miR-466i-5p, mmu-miR-342-3p, mmu-let7i-5p, mmu-miR-34a-5p, mmu-miR-188-5p and mmu-miR-5119) were upregulated and the other five (mmu-miR-378a-3p, mmu-miR-202-3p, mmu-miR-378b, mmu-miR-378d and mmu-miR-212-3p) were downregulated in the CCl [4] group compared with the control (Fig. 1a,b). [score:6]
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[+] score: 5
Other miRNAs from this paper: mmu-mir-188
More recently, FGF5 was identified as a critical target of the tumor suppressive microRNA-188-5p in hepatocellular carcinoma [22]. [score:5]
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[+] score: 5
Results showed that miR-323b-5p, miR-221-3p, miR-524-5p, and miR-188-3p were underexpressed in albuminuric relative to nonalbuminuric patients, while miR-214-3p, miR-92b-5p, hsa-miR-765, hsa-miR-429, miR-373-5p, miR-1913, and miR-638 were overexpressed [71]. [score:5]
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[+] score: 5
[14, 15] MiR-135a*, miR-188-5p, miR-663 and miR-483-5p were downregulated in plasma cell leukemia. [score:4]
At the same time, many other miRNAs were unmasked, including miR-125a-3p, miR-155, miR-135a*, miR-198, miR-200c, miR-188-5p, miR-630, miR-663 and miR-483-5p. [score:1]
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[+] score: 5
Fang F MicroRNA-188-5p suppresses tumor cell proliferation and metastasis by directly targeting FGF5 in hepatocellular carcinomaJ. [score:5]
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[+] score: 5
Other APP-interacting proteins, APP -binding family B member 1 (mir-9, miR-340, and miR-135b), APP -binding family member 2 (let-7 and miR-218), and APP -binding family 2 (miR-188 and miR-206) were also predicted targets, some of which had near exact target site matches. [score:5]
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[+] score: 4
Other miRNAs from this paper: hsa-mir-567
Moreover, FGF5 is a direct target of miR-188-5p in hepatocellular carcinoma (HCC) and acts as an oncogene in HCC and glioblastoma multiforme (Allerstorfer et al., 2008[1]; Fang et al., 2015[7]). [score:4]
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[+] score: 4
Wu J. Lv Q. He J. Zhang H. Mei X. Cui K. Huang N. Xie W. Xu N. Zhang Y. MicroRNA-188 suppresses G1/S transition by targeting multiple cyclin/CDK complexes Cell Commun. [score:4]
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[+] score: 4
For H1N1 infected cells, at 18 and 24-hour post-infection, miR-188-5p, miR-1260, miR-1274a, miR-1274b, miR141, miR183*, miR-18b, miR-19a, miR21*, miR-301a, miR-572, miR-720, and miR-939 were found to be up-regulated (>1.5-fold, p<0.05) (Table 1). [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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[+] score: 3
Lin et al reported that the high let-7a-2-3p and low miR-188-5p expression could be potentially used as favorably prognostic biomarkers independently in CN-AML patients [9]. [score:3]
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[+] score: 3
In summary, the ceRNA network suggested that novel_circRNA_007362 and novel_circRNA_032232 might interact with 24 miRNAs (Fig. 6A) as well as tch-let-7a-3p, tch-miR-136-5p, tch-miR-146a-5p, tch-miR-17-5p, tch-miR-183-5p, tch-miR-188-5p, tch-miR-23b-3p, tch-miR-326, and tch-miR-93-5p (Fig. 6B) to regulate development and aging of the cerebellum and hippocampus. [score:3]
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[+] score: 3
Furthermore, miR-188-5p was analyzed by performance of an experiment in aggressive RASF and long-time cultivated RASF (less aggressive); they were both challenged with IL-1 β and TNF- α; aggressive RASF showed a 20% decreased miR-188-5p expression, after both challenges, and was associated with diminished migration patterns [55]. [score:3]
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[+] score: 2
Namely, pregnant rats fed SO and FO diets during the first 12 days of pregnancy showed significant lower expression of miR-449c-5p, miR-134–5p, miR-188, miR-32, miR130a, miR-144–3p, miR-431, miR-142–5p, miR-33, miR-340–5p, miR-301a, miR-30a, miR-106b, and miR-136–5p, as compared with OO, LO, and PO diets. [score:2]
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[+] score: 2
MiRNA-188-5p suppresses cancer cell proliferation and metastasis in vitro and in vivo by interacting with fibroblast growth factor 5 (FGF5) [76]. [score:2]
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[+] score: 2
Other miRNAs from this paper: hsa-mir-17, hsa-mir-28, hsa-mir-223, hsa-mir-127, hsa-mir-194-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-30e, hsa-mir-362, hsa-mir-363, hsa-mir-367, hsa-mir-379, hsa-mir-196b, hsa-mir-450a-1, hsa-mir-431, ssc-mir-28, hsa-mir-493, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-500a, hsa-mir-501, hsa-mir-502, hsa-mir-450a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-506, hsa-mir-508, hsa-mir-509-1, hsa-mir-532, hsa-mir-615, hsa-mir-660, bta-mir-127, bta-mir-30e, bta-mir-17, bta-mir-450a-2, bta-mir-532, bta-mir-363, bta-mir-660, hsa-mir-891a, hsa-mir-892a, hsa-mir-509-2, hsa-mir-450b, hsa-mir-892b, hsa-mir-708, hsa-mir-509-3, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1248, ssc-mir-17, bta-mir-155, bta-mir-188, bta-mir-194-2, bta-mir-196b, bta-mir-223, bta-mir-28, bta-mir-362, bta-mir-367, bta-mir-379, bta-mir-431, bta-mir-493, bta-mir-500, bta-mir-502a-1, bta-mir-502a-2, bta-mir-502b, bta-mir-615, bta-mir-708, bta-mir-1248-1, bta-mir-1248-2, ssc-mir-450a, bta-mir-2320, bta-mir-1388, bta-mir-194-1, bta-mir-450a-1, eca-mir-30e, eca-mir-367, eca-mir-684, eca-mir-196b, eca-mir-615, eca-mir-708, eca-mir-194-1, eca-mir-493a, eca-mir-17, eca-mir-1248, eca-mir-28, eca-mir-127, eca-mir-379, eca-mir-431, eca-mir-493b, eca-mir-155, eca-mir-194-2, eca-mir-188, eca-mir-223, eca-mir-362, eca-mir-363, eca-mir-450a, eca-mir-450b, eca-mir-450c, eca-mir-500-1, eca-mir-500-2, eca-mir-501, eca-mir-502, eca-mir-508, eca-mir-509a, eca-mir-532, eca-mir-660, ssc-mir-30e, ssc-mir-196b-1, ssc-mir-450b, ssc-mir-127, ssc-mir-532, ssc-mir-708, ssc-mir-1285, ssc-mir-500, hsa-mir-514b, ssc-mir-363-1, ssc-mir-450c, hsa-mir-500b, ssc-mir-194b, ssc-mir-155, ssc-mir-362, bta-mir-3601, ssc-mir-615, ssc-mir-2320, bta-mir-450b, ssc-mir-194a, ssc-mir-196b-2, ssc-mir-363-2, ssc-mir-493, hsa-mir-892c, eca-mir-1388, eca-mir-514b, eca-mir-506a, eca-mir-509b, bta-mir-194b, ssc-mir-1388, ssc-mir-223, ssc-mir-660, bta-mir-194b-2, bta-mir-1949
In pig we found a cluster on chrX of mir-532, mir-188, mir-500, mir-362, mir-500, mir-660, and a mature unknown miRNA picked up by miRDeep. [score:1]
A more difficult case is the mir-532 cluster located on chrX in human (Additional file 1: Figure S14), which contains 8 known miRNAs from miRBase: mir-532, mir-188, mir-500a, mir-362, mir-501, mir-500b, mir-660, mir-502. [score:1]
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[+] score: 2
Pre-clinical studies in healthy mice and in vitro studies using estrogen have identified miRNAs either regulated by estrogen (miR-203, miR-126, miR-23a, miR-21, miR-24, miR-27a and b, and miR-106a and b) or encoded by X-chromosome (miR-98, miR-652, miR-221, miR-222, miR-223, miR-361, miR-421, miR-325, miR-188, miR-92a, miR-424, miR-503, miR-505). [score:2]
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43
[+] score: 2
Other miRNAs from this paper: 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-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-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-98, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-199a-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-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-222, hsa-mir-223, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, 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-127, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-363, hsa-mir-302c, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-328, hsa-mir-342, hsa-mir-326, hsa-mir-135b, hsa-mir-338, hsa-mir-335, hsa-mir-345, hsa-mir-424, hsa-mir-20b, hsa-mir-146b, hsa-mir-520a, hsa-mir-518a-1, hsa-mir-518a-2, hsa-mir-500a, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-92b, hsa-mir-574, hsa-mir-614, hsa-mir-617, hsa-mir-630, hsa-mir-654, hsa-mir-374b, hsa-mir-301b, hsa-mir-1204, hsa-mir-513b, hsa-mir-513c, hsa-mir-500b, hsa-mir-374c
This study also uncovered a novel set of miRNAs like miR-222 and let-7f (associated with other malignancies), miR-513 and miR-223 (linked to immune regulation and related B-cell tumors), miR-424 (hematopoiesis), and miR-188 and miR-374 (no known physiological or pathological functions) [49]. [score:2]
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44
[+] score: 2
Among these, ten were significantly up- regulated in megakaryocytes with the top four being miR1246, miR-148a, miR-22 and miR-188 from 18 to 5 fold increase. [score:2]
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45
[+] score: 2
Other miRNAs from this paper: hsa-mir-296, hsa-mir-328, hsa-mir-331, hsa-mir-432
Mir-432, Mir-188, and Mir-331 target each have putative binding sites in the 3' UTR of >8 EC-restricted genes. [score:2]
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46
[+] score: 1
MiR-140-5p in plasma was negative correlated to hemoglobin while plasma miR-188-5p was positive correlated to hemoglobin. [score:1]
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47
[+] score: 1
Among the cancer-related miRNAs, five miRNAs, namely, hsa-mir-217, hsa-mir-188, hsa-mir-125b-1, hsa-mir-100, and hsa-mir-181d, were reported to be associated with the acute myeloid leukemia. [score:1]
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48
[+] score: 1
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-200c, hsa-mir-483
Pichler M. Stiegelbauer V. Vychytilova-Faltejskova P. Ivan C. Ling H. Winter E. Zhang X. Goblirsch M. Wulf-Goldenberg A. Ohtsuka M. Genome-Wide miRNA Analysis Identifies miR-188–3p as a Novel Prognostic Marker and Molecular Factor Involved in Colorectal CarcinogenesisClin. [score:1]
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49
[+] score: 1
This analysis identified 7 candidate miRs that were clearly above all the other miRs: hsa-miR-630, hsa-miR-302d-3p, hsa- miR-320e, hsa-miR-612, hsa-miR-378e, hsa-miR-25-3p, hsa- miR-188-5p. [score:1]
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50
[+] score: 1
45 (49) SLC2A3, SCARA3, ORAI2, MBOAT2, C9ORF910.0113HSA-MIR-188–3P. [score:1]
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51
[+] score: 1
Pichler M. Stiegelbauer V. Vychytilova-Faltejskova P. Ivan C. Ling H. Winter E. Zhang X. Goblirsch M. Wulf-Goldenberg A. Ohtsuka M. Genome-wide microRNA analysis identifies miR-188–3p as novel prognostic marker and molecular factor involved in colorectal carcinogenesis Clin. [score:1]
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52
[+] score: 1
Pichler M. Stiegelbauer V. Vychytilova-Faltejskova P. Ivan C. Ling H. Winter E. Zhang X. Goblirsch M. Wulf-Goldenberg A. Ohtsuka M. Genome-Wide miRNA Analysis Identifies miR-188-3p as a Novel Prognostic Marker and Molecular Factor Involved in Colorectal CarcinogenesisClin. [score:1]
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53
[+] score: 1
Each clusters had at least 2 genes, with miR-532∼miR-188 cluster in chromosome X having 2 genes, and mir-363∼106a cluster having 6 genes. [score:1]
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54
[+] score: 1
We observe a similar situation for another cluster on human chromosome X: hsa-mir-188, HN-11, HP-77, HN-12, and HN-13 (in transcription sense order). [score:1]
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55
[+] score: 1
Other miRNAs from this paper: hsa-mir-22, hsa-mir-140, hsa-mir-372, hsa-mir-507
Pichler M. Stiegelbauer V. Vychytilova-Faltejskova P. Ivan C. Ling H. Winter E. Zhang X. Goblirsch M. Wulf-Goldenberg A. Ohtsuka M. Genome-wide miRNA analysis identifies miR-188-3p as a novel prognostic marker and molecular factor involved in colorectal carcinogenesisClin. [score:1]
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56
[+] score: 1
In this study, we used time-lapse video microscopy to observe cell movement in the scratch-wound assay, validated the results using the transwell migration assay, and identified the migration-suppressing miRNA (miR-134) and migration-facilitating miRNAs (miR-1247, miR-1244, miR-146b-3p, miR-1471, miR-188-3p, miR-661, miR-891a, miR-891b and miR-767-5P) in SK-HEP-1 cells. [score:1]
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57
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CCR-17-0023 28533224 4. Picler M. Stiegelbauer V. Vychytilova-Faltejskova P. Ivan C. Ling H. Winter E. Zhang X. Goblirsch M. Wulf-Goldenberg A. Ohtsuka M. Genome-wide miRNA analysis identifies miR-188-3p as a novel prognostic marker and molecular factor involved in colorectal carcinogenesisClin. [score:1]
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2012.35 22491495 8. Li C. J. Cheng P. Liang M. K. Chen Y. S. Lu Q. Wang J. Y. Xia Z. Y. Zhou H. D. Cao X. Xie H. MicroRNA-188 regulates age-related switch between osteoblast and adipocyte differentiationJ. [score:1]
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