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70 publications mentioning hsa-mir-491

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-491. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 254
miR-491 mimics or scrambled miRNA controls were synthesized to knock down the expression of miR-491 and western-blot assay showed miR-491 mimics markedly suppressed TRIM28 expression at protein level (Fig.   3a and b). [score:7]
As a result, up-regulation of miR-491 suppressed proliferation ability of glioma cells, which could be reversed by restoration of TRIM28. [score:6]
miR-491 directly binds to 3’UTR of TRIM28 mRNA and suppresses TRIM28 expression. [score:6]
Down-regulation of miR-491 lead to enhanced expression of TRIM28 and promote the proliferation of glioma cells. [score:6]
Transfection of U87 and U251 cells with miR-491 mimics lead to up-regulated expression of miR-491 and an obvious reduction of TRIM28 protein level in both cell lines. [score:6]
Literature also demonstrated that TRIM28 was one of the 681 genes potentially targeted by miR-491 predicted by Targetscan, but without further verified [12]. [score:5]
Our present study indicated an aberrant expression of miR-491 in GBM specimens and that TRIM28 protein levels negatively correlates with miR-491 expression from TCGA database and our cohort. [score:5]
mRNA target sites of miR-491 was predicted through the algorithms TargetScan Human 5.1 (www. [score:5]
c Spearman’s correlation analysis of miR-491 expressions and TRIM28 protein levels (r = -0.2323, P = 0.0044) miR-491 has been reported to suppress the proliferation of U251 cell lines. [score:5]
X Li et al. [12] indicated that miR-491-5p could modulate the expression of Bcl-xL, CDK6 and EGFR, meanwhile CDK6 and IGFBP2 were the target of miR-491-3p. [score:5]
Several studies indicated that miR-491-5p expression was reduced and acted as a potential cancer suppressor in various cancers, for instance, hepatocellular carcinoma, ovarian carcinoma, oral squamous cell carcinoma and pancreatic cancer [11, 17– 19]. [score:5]
Via inhibition of Epithelial-Mesenchymal Transition (EMT) and expression of matrix metalloproteinase, miR-491 is also related to metastasis of hepatocellular carcinoma [11]. [score:5]
Clone formation and MTT assays indicated that up-regulation of miR-491 inhibited the proliferation of glioma cells. [score:5]
Loss of MIR-491 could regulate IGFBP2, CDK6 and EGFR proliferative pathways, by which the propagation of GBM cancer stem cells was inhibited. [score:4]
In conclusion, our present study indicates a common phenomenon that miR-491 is down-regulated in GBM and miR-491 is proved to be involved in modulating proliferation of glioma cells in vitro. [score:4]
We demonstrate that TRIM28 is a direct target of miR-491. [score:4]
Then we predicted possible mRNA target of miR-491 by TargetScan/MicroRNA and confirmed it via luciferase reporter assays. [score:4]
Above results indicated that TRIM28 is direct target of miR-491. [score:4]
miR-491 regulates glioma cells proliferation in vitro by targeting TRIM28. [score:4]
Several studies indicated a correlation between the downregulation of miR-491 and tumor malignancy in GBM [12, 13]. [score:4]
As far as we know, this study confirmed that miR-491 directly targets TRIM28 in modulating proliferation activity of glioma cells in vitro for the first time. [score:4]
There was a positive correlation between the down-regulation of miR-491 and poor prognosis. [score:4]
So the close relevance of spatial structure and regulatory relationship between MIR-491 and the wi dely recognized cancer related genes mentioned above indicated the tumor inhibition ability of miR-491 in GBM. [score:4]
Nakano et al. demonstrated that miR-491 was up-regulated in colorectal cancer and induced apoptosis via the modulation of Bcl-XL [10]. [score:4]
TRIM28 protein was obviously up-regulated in U87 and U251 cells after transfection with miR-491, which also confirmed above conclusion. [score:4]
Fig. 2TRIM28 is directly targeted by miR-491. [score:4]
miR-491 is obviously down-regulated in glioma tissues and cell lines, which is correlated with poor prognosis. [score:4]
Cell transfections with plasmid vectors expressing TRIM28, pLenti-TRIM28 or miR-491 mimics (Genomeditech, Shanghai, China) were carried out with Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). [score:3]
miR-491 and Tripartite motif containing 28 (TRIM28) are reported to aberrantly express in glioblastoma multiforme (GBM). [score:3]
Here, we detected miR-491 and TRIM28 expression and function in glioma cells. [score:3]
TRIM28 is the target of miR-491. [score:3]
miR-491 expression were examined bys. [score:3]
Above results may indicate that miR-491 may serve as tumor suppressor gene in glioma. [score:3]
miR-491 expression, OS and PFS of 512 GBM tissues from TCGA database. [score:3]
We wondered whether TRIM28 played any role in miR-491 mediated inhibition of glioma cell proliferation. [score:3]
Loss of MIR-491 is negatively correlated with the overexpression of IGFBP2, CDK6, and EGFR. [score:3]
P = 0.0055 Following searching for TargetScan and human microRNA database, we found the possible complementary base pair between seed region of miR-491 and nucleotide 57–63 region in the 3’-UTR of TRIM28 (Fig.   2a). [score:3]
miR-491 expressed lower in glioma cell lines SHG-44 (low grade), U87 and U251 (high grade) than normal brain specimens(* P < 0.05,** P < 0.01) (Fig.   1b). [score:3]
Then, we confirmed that TRIM28 was a direct target of miR-491 via a luciferase assay. [score:3]
miR-491 inhibits glioma cell proliferation by modulating TRIM28. [score:3]
To determine sequence specificity, we also established the plasmids pGL3-TRIM28-mt in which the conserved targeting sequence of miR-491 was mutated to 5’-GUAAAGA-3’. [score:3]
Spearman’s correlation analysis demonstrated that miR-491 expression was negatively correlated with TRIM28 protein level. [score:3]
miR-491 expression correlated negatively with TRIM28 protein levels. [score:3]
We synthesized the 3’UTR of TRIM28 containing the miR-491 target sequence (5’-UCCCCAC-3’) (Genomeditech, Shanghai, China) and inserted it into pGL3-control vector (Promega, Madison, WI), with resultant plasmids pGL3-TRIM28-wt. [score:3]
Optimal cut-off for miR-491 expression based on survival analysis was obtained by using X-tile software version 3.6.1 (Yale University School of Medicine, New Haven, CT, USA) [16]. [score:3]
P < 0.0001. d Retrospective analysis of the overall survival from TCGA database demonstrated that decreased miR-491 expression represent poor prognosis in GBM. [score:3]
It showed that miR-491 expressed lower in GBM tissues (*** P < 0.001) (Fig.   1a). [score:3]
Next, we tested miR-491 expression levels in several glioma cell lines and got the similar results as shown in glioma tissues. [score:3]
Interestingly, MIR-491’s host gene, KIAA1797/FOCAD, was well recognized to function as tumor suppressor gene of glioma. [score:3]
We analyzed miR-491 expressions in 20 primary human GBM tissues and 6 control brain tissues bys and searched for The Cancer Genome Atlas (TCGA) database. [score:3]
According to above results, we supposed miR-491 to serve as a tumor suppressor in glioma. [score:3]
The result demonstrate that miR-491 was low expressed in GBM tissues. [score:3]
3’ UTR of MMP-9 was directly targeted by miR-491-5p, which was verified by luciferase assay [13]. [score:3]
miR-491-5p were demonstrated to be negatively correlated with the expression of MMP-9 protein and reduced invasive ability of U251 and U87 glioma cell lines. [score:3]
Moreover, MIR-491 is indicated always deleted together with CDKN2A, a tumor suppressor gene famous for encoding p16 [INK4α] and p14 [ARF]. [score:3]
TCGA database also indicated a significant lower miR-491 expression in GBM (n = 512) than in control brain tissues (n = 10) (P < 0.0001) (Fig.   1c). [score:3]
miR-491 expression was obviously reduced in GBM cells and tissues. [score:3]
Just because the important part miR-491 plays in gliomas and its possible regulation relationship with TRIM28, we conducted further researches. [score:2]
These data indicated that miR-491 regulated the proliferation capability of gliomas cells via TRIM28. [score:2]
Knock-down of miR-491 and transfection of pLenti-TRIM28 were performed in U251 and U87 cells. [score:2]
Above findings suggested that TRIM28 was regulated in GBM tissues and cells by miR-491. [score:2]
Next, we synthesis the 3’UTR of TRIM28 containing miR-491 binding sites and a luciferase reporter gene, then inserted it into a pGL3 vector to confirm the direct interaction between miR-491 and the 3’UTR of TRIM28 (Fig.   2c). [score:2]
Possible mRNA binding sites of miR-491 predicted by TargetScan/MicroRNA were proved by luciferase assays. [score:2]
miR-491 negatively regulates TRIM28 levels in GBM. [score:2]
a Expression of miR-491 in GBM tissues (n = 20) and control brain tissues (n = 6) tested by RT-qPCR assays. [score:2]
Glioblastoma miR-491 TRIM28 Proliferation Proteins of TRIM family belong to members of E3 ligases family, which play an important part in the process of cellular protein hydrolysis [1]. [score:1]
miR-491-5p and miR-491-3p are two mature miRNAs produced by MIR-491. [score:1]
MTT assay (Fig.   4b) and clone formation (Fig.   4c) assay indicated that up-regulation of miR-491 decreased proliferation capacity of U251 and U87 glioma cells compared with NC -transfected. [score:1]
This study indicates that miR-491 may serve as a potential diagnostic marker of GBM and restoration of miR-491 together with other combined treatments, may develop into an effective method for the treatment of gliomas. [score:1]
As a result, restoration of miR-491 together with other combined treatments may develop into an effective method for the treatment of gliomas. [score:1]
BibiServ analysis showed that the free energy (DG) was approximately -29.5 kcal/mol for hybridization of the TRIM28 3’-UTR and miR-491 (Fig.   2b). [score:1]
a U251 and U87 cells were transfected with miR-491 mimics or scrambled miRNA (miR-NS). [score:1]
HEK-293 cells were co -transfected with miR-491 mimics or scrambled miRNA and reporter plasmids using Lipofectamine 2000. [score:1]
Several literatures have elucidated the role which miR-491 plays in tumorigenesis and tumor progression. [score:1]
In the present study, we investigated miR-491 expression and TRIM28 level in both our cohort and from The Cancer Genome Atlas (TCGA) database. [score:1]
What’s more, retrospective analysis of the clinical outcome from TCGA data demonstrated a positive correlation between decreased miR-491 and poor survival in GBM (P = 0.0055) (Fig. 1d). [score:1]
Meanwhile, miR-491 may influence proliferation ability of glioma cells partly through p21 pathway. [score:1]
In order to test the assumption, we constructed miR-491 transfected cell lines to performed functional analyses. [score:1]
a U251 and U87 cells were transfected with scrambled microRNA (NC), miR-491 mimics or miR-491 mimics together with pLenti-TRIM28. [score:1]
Next, we searched for TCGA data to investigate the relationship between expression of TRIM28 and miR-491 level. [score:1]
a The nucleotide 57-63 region within the 3’-UTR of TRIM28 are potential complementary site of miR-491. [score:1]
It showed that Luciferase activities in the group transfected with pGL3-TRIM28-wt and miR-491 mimics is significant lower than that in other groups (*** P < 0.001). [score:1]
d were performed after co-transfecting with pGL3-TRIM28-wt or pGL3-TRIM28-mt alone, or together with miR-491 mimics or scrambled miRNA controls (NS). [score:1]
b BibiServ analysis of free energy (DG) for hybridization of miR-491 and 3’-UTR of TRIM28. [score:1]
Deletion of MIR-491 has been recently reported to modulate the invasion and proliferation of GBM [12]. [score:1]
were performed following co-transfecting with pGL3-TRIM28-wt or pGL3-TRIM28-mt alone, or together with miR-491 mimics or scrambled miRNA controls (NS) (Fig.   2d). [score:1]
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We found that both Rcitor knockdown and treatment with an mTOR inhibitor led to significant increase of miR-491-3p expression in Tca8113/PYM cells (Figure 5A), whereas elevated expression of Rictor downregulated miR-491-3p expression in Tca8113, SCC-25 and CAL-27 cell lines (Figure 5B). [score:13]
Notably, transfection with miR-491-3p mimics significantly downregulated Rictor protein level in Tca8113/PYM cells, and the miR-491-3p inhibitor clearly upregulated Rictor protein level in Tca8113, SCC-25 and CAL-27 cell lines (Figure 3D). [score:9]
The mTORC2 signaling pathway downregulates miR-491-3p expression via inhibiting the transcriptional activation of FOXO1. [score:8]
More importantly, we uncover a reduced expression of miR-491-3p in the majority of tongue cancer tissues and its downregulation significantly predicts for a poor prognosis of overall survival in tongue cancer patients. [score:6]
Here, we showed that Rictor was overexpressed accompanied with increased mTORC2 activation due to miR-491-3p downregulation in drug resistant tongue cancer cells. [score:6]
To assess whether Rictor is a direct target of miR-491-3p, a luciferase reporter vector containing the putative Rictor 3′UTR target site for miR-491-3p (pMir-Wt, as wildtype version) or a mutant version with a deletion of 7bp in the seed sequence was constructed (pMir-Mut). [score:6]
Because of the significant reduction of miR-491-3p leading to Rictor upregulation in Tca8113/PYM cells, the expression levels of Rictor and mTORC2 activity were much higher in Tca8113/PYM cells than that in Tca8113, SCC-25 and CAL-27 cell lines, which was reflected by the levels of phosphorylated Akt(Ser473), SGK1(Ser422), FOXO1(Thr24) (Figure 3C). [score:6]
On the other hand, Rictor protein was highly expressed in only 5 (22.7%) of 22 tongue cancer tissues with relative high expression of miR-491-3p (Figure 6B), suggesting an inverse correlation between miR-491-3p and Rictor in tongue cancers. [score:5]
In contrast the luciferase activity from wildtype version in Tca8113/PYM cells was higher than that in Tca8113, SCC-25 and CAL-27 cells (Figure 3E), suggesting that endogenous miR-491-3p inhibits Rictor expression by binding to the seed sequence in the 3′UTR of Rictor mRNA. [score:5]
Overexpression of miR-491-3p inhibited glioma cell invasion and proliferation and impaired the propagation of glioma stem cells [20]. [score:5]
Inversely, the sensitivity of Tca8113 (Figure 2B), SCC-25 (Figure 2C) and CAL-27 (Figure 2D) cells to PYM or cDDP was dramatically decreased upon inhibition of miR-491-3p with specific inhibitor, accompanied with reduced apoptosis -induced by PYM or cDDP. [score:5]
Moreover, tongue cancer patients with low levels of miR-491-3p and highly expressed Rictor exhibited a significantly worse overall survival than the patients with high levels of miR-491-3p and reduced expression of Rictor (Figure 6E). [score:5]
These data demonstrated a negative expression pattern between miR-491–39 and Rictor or mTORC2 activity, indicating that miR-491-3p might target Rictor mRNA in vivo as well. [score:5]
Conversely, ectopic expression of Rictor not only decreased the binding of FOXO1 to the promoter of miR-491-3p (Figure 5F), it also significantly suppressed the promoter activity in Tca8113, SCC-25 and CAL-27 cell lines (Figure 5I). [score:5]
miR-491-3p expression correlated with Rictor expression and mTORC2 activity in tongue cancer, associating with prognosis of tongue cancers patients. [score:5]
mTORC2 signal inhibits miR-491-3p expression via FOXO1 inactivation. [score:5]
mTORC2 inhibits miR-491-3p expression via modulation of FOXO1 activation. [score:5]
Inversely, miR-491-3p inhibitor increased the luciferase activities from the wildtype version, and the mutant version abrogated the facilitative effect of miR-491-3p inhibitor (Figure 3F). [score:5]
Restored expression of miR-491-3p sensitized Tca8113/PYM cells to chemotherapy, whereas functional inhibition of miR-491-3p led to enhanced resistance of tongue cancer cells to chemotherapy. [score:5]
miR-491-3p directly targets Rictor, a component of mTORC2 complex. [score:4]
As to cancer, miR-491-3p was found to be downregulated in retinoblastoma cells under hypoxic condition, which is an essential feature of retinoblastoma and contributes to poor prognosis and resistance to conventional therapy [19]. [score:4]
Functional interference of miR-491-3p negatively regulated Rictor protein expressionand the mTORC2 activity (Figure 3D). [score:4]
We found that miR-491-3p was significantly downregulated in Tca8113/PYM cells. [score:4]
Importantly, tongue cancer patients with low expression of miR-491-3p have a poorer prognosis for overall survival as compared to the patients with high expression of miR-491-3p (Figure 6C). [score:4]
Moreover, both Rictor knockdown and inhibition of mTOR activity with KU-0063794 promoted FOXO1 binding to miR-491-3p promoter at site A and site D (Figure 5E). [score:4]
Furthermore, we demonstrated the expression of miR-491-3p could be transcriptionally regulated by FOXO1, which was inactivated by mTORC2. [score:4]
In the present study, miR-491-3p was found to be downregulated in PYM -induced multidrug resistant tongue cancer cells termed as Tca8113/PYM. [score:4]
Figure 6 (A) Representative images of miR-491-3p expression detected by ISH (red staining as nucleus and blue staining as miR-491-3p level) and Rictor, p-Akt, p-SGK1 and p-FOXO1 protein levels detected by immunohistochemical staining in tongue cancer tissues (20×). [score:3]
miR-491-3p repressed Rictor protein expression. [score:3]
org) to predict potential targets of miR-491-3p. [score:3]
Figure 2 (A) overexpressed miR-491-3p via transfection of miR-491-3p mimics sensitized Tca8113/PYM cells to PYM and cDDP, detected by to determing proliferation and hochest stain to determining apoptosis respectively. [score:3]
miR-491-3p mimics, miR-491-3p inhibitor, and relative controls were purchased from Exiqon (Vedbaek, Denmark). [score:3]
The results from luciferase reporter assays confirmed that Rictor was a direct target of miR-491-3p in tongue cancer. [score:3]
The miR-491-3p expression in tongue cancer samples was detected by In Site Hybridizations (ISH) with kit from Exiqon (Vedbaek Denmark) according to the manufacturer's instructions. [score:3]
These results strongly demonstrated the specificity of miR-491-3p targeting Rictor mRNA. [score:3]
MiR-491-3p expression was significantly down regulated in the chemo-resistant Tca8113/PYM cells. [score:3]
Our studies determined a negative feedback loop between miR-491-3p expression and mTORC2 activity through the transcription factor FOXO1. [score:3]
Figure 5 (A and B) Relative mean expression of miR-491-3p was determined by qRT-PCR. [score:3]
Cells were seeded in 96 well-plates and co -transfected with pMir-Report luciferase vector, pRL-TK Renilla luciferase vector and miR-491-3p mimics or inhibitor using Lipofectamine 2000 (Invitrogen). [score:3]
It is suggested that new strategies with targeted intervention on this miR-491-3p/mTORC2 axis may significantly enhance the efficacy of chemotherapy against human tongue cancer. [score:3]
As shown in Figure 1C, miR-491-3p expression was relatively higher in chemo-sensitive SCC-25 and CAL-27 tongue cancer cell lines than that in Tca8113/PYM cells. [score:3]
Importantly, restored expression of miR-491-3p re-sensitized Tca8113/PYM cells to the treatment of PYM and cisplatin (cDDP). [score:3]
These results suggest that miR-491-3p plays a tumor suppressive role in tongue cancer. [score:3]
Increased miR-491-3p via transfection of miR-491-3p mimics significantly enhanced the sensitivity of Tca8113/PYM cells to PYM- and cDDP -induced growth inhibition and apoptosis (Figure 2A). [score:3]
Recently, Li et al. observed that miR-491-3p was downregulated in glioblastoma multiforme samples as compared to the normal brain tissues. [score:3]
Remarkably, ISH results demonstrated that 62 (73.81%) tongue cancer tissues exhibited relative low expression of miR-491- 3p. [score:3]
MiR-491-3p appeared to exert its effect via regulating Rictor expression in mTORC2 complex. [score:3]
Conversely, inhibition of miR-491-3p reduced the sensitivity of Tca8113, SCC-25 and CAL-27 cells to chemotherapy. [score:3]
s confirmed the direct transcriptional regulation of miR-491-3p by FOXO1. [score:3]
In contrast, overexpression of Rictor attenuated the binding of FOXO1 to miR-491-3p promoter in Tca8113, SCC-25 and CAL-27 cell lines (Figure 4F), associated with an increased p-FOXO1 (Figure 4C). [score:3]
We also found the level of p-FOXO1 increased in tongue cancer cell lines and clinical samples with high Rictor and mTORC2 activity and low expression levels of miR-491-3p. [score:3]
Thus, we next investigated the potential feedback regulation of miR-491-3p expression by mTORC2. [score:2]
Our data suggest a negative regulatory loop between mTORC2 signaling and miR-491-3p mediated by FOXO1 in chemo-resistant tong cancer cells. [score:2]
Given the feedback regulatory loop between miR-491-3p and mTORC2 activity identified in our cell culture studies, we wondered whether the miR-491-3p/mTORC2 axis might associate with the prognosis of tongue cancer patients. [score:2]
We found that the luciferase activity driven by the potential promoter of miR-491-3p was much higher in Tca8113, SCC-25 and CAL-27 cell lines than that in Tca8113/PYM cells (Figure 5G). [score:1]
miR-491-3p modulates chemosensitivity in tongue cancer cells. [score:1]
Moreover, miR-491-3p mimics significantly repressed the luciferase activity of the vector with wild-type Rictor 3′UTR in Tca8113/PYM cells, but the mutant version abrogated the repressive ability of miR-491-3p (Figure 3F). [score:1]
Our clinical studies support that the miR-491-3p/mTORC2 axis associates with the prognosis of tongue cancer patients. [score:1]
After dehydration in ethanol, sections were hybridizated with 40 nM double-DIG LNA™ miR-491-3p probe 55°C for 1 h. After wash in SSC buffer at hybridization temperature and incubation with blocking solution for 15 min, the anti-DIG reagent sheep anti-DIG-AP (Roche, Mannheim, Germany) was applied and incubated for 60 min at RT. [score:1]
To validate the direct association of FOXO1 with the promoter of miR-491-3p, we performed assays and discovered that FOXO1 most significantly bound to site A and site D. The bindings in Tca8113/PYM cells were much lower than those in the chemo-sensitive tongue cancer cell lines (Figure 5D). [score:1]
The expression levels of miR-491-3p and several components of mTORC2 signaling pathway were evaluated in clinical samples of tongue cancer patients. [score:1]
We performed in situ hybridizations (ISH) to detect miR-491-3p and immunohistochemical staining to examine Rictor, p-Akt(Ser473), p-SGK1(Ser422) and p-FOXO1(Thr24) in the tissues from 84 tongue cancer patients who received chemotherapy based on PYM and/or cDDP. [score:1]
In summary, as shown in Figure 6F, our studies demonstrated an important role of the negative feedback between miR-491-3p and mTORC2 signaling mediated by Rictor and FOXO1 in drug resistance of tongue cancer. [score:1]
Taken together, these results strongly support that FOXO1 physically binds to the promoter region of miR-491-3p to drive its transcription. [score:1]
The mTORC2 component Rictor with a conserved binding site of miR-491-3p was selected for further identification (Figure 3A). [score:1]
Our current studies revealed an inverse correlation between miR-491-3p and Rictor in tongue cancer cell lines and clinical samples. [score:1]
Bioinformatics analysis combined with uncovered the physical binding of FOXO1 to the miR-491-3p promoter in tongue cancer cells. [score:1]
MiR-491-3p was thought to play a potential role in regulating meiotic recombination- and synapsis-related genes [18]. [score:1]
Figure 3 (A) Schematic of predicted miR-491-3p site in the 3′UTR of human Rictor mRNA, which broadly conserved among vertebrates. [score:1]
miR-491-3p sensitized tongue cancer cells to chemotherapy. [score:1]
For promoter activity assay: To determine whether FOXO1 regulates the promoter activity of miR-491-3p, a two kilobase region upstream of the miR-491-3p precursor starting site was cloned into the pGL4-reporter vector upstream of the luciferase gene. [score:1]
We then analyzed the response elements of a cohort of transcription factors located within 2kb region upstream of miR-491-3p precursor start site using the online software “The JASPAR database”. [score:1]
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As shown in Figure 3a, inhibition of PI3K/AKT by LY294002 resulted in increased miR-491-5p expression as early as 1.5 h after treatment. [score:5]
We used small molecule inhibitors (SMI) to examine signalling pathways that exert miR-491-5p inhibitory effect of TFF3. [score:5]
Our results show that TFF3 inhibits miR-491-5p expression in HT-29/B6 cells thus reducing cellular levels of PRINS. [score:5]
Treatment with IFN- γ/TNF- α as described above slightly enhanced miR-491-5p expression in TFF3 -overexpressing clones of HT-29/B6 cells (Figure 1h). [score:5]
Downregulation of several miRNAs became apparent on day 7; miR-155, miR-326, miR-329 and miR-491 exhibited clearly (≤0.67-fold changes) and significantly decreased expression (P<0.05) compared with mock controls (Figure 1c and Supplementary Figures 1c and d). [score:5]
We concentrated on miR-155, miR-326, miR-329 and miR-491-5p showing stable downregulation after prolonged incubation. [score:4]
[39] In our study, TFF3 -dependent downregulation of miR-491-5p caused accumulation of PRINS. [score:4]
In conclusion, TFF3 exerts its anti-apoptotic effects by means of AKT/PI3K -dependent miR-491-5p downregulation and increased levels of PRINS in HT-29/B6 cells. [score:4]
Chemical PI3K/AKT inhibition and consequently increased miR-491-5p efficiently reduced cellular PRINS levels compared with untreated HT-29/B6/TFF3 cells without effects on TFF3 expression (Figure 3d). [score:4]
The collection included three well-known miRNAs (miR-16, miR-21 and miR-155) that have been commonly related to apoptotic signalling and cancer, [28–30] as well as three underexplored miRNAs (miR-326, miR-329 and miR-491) with accumulated targets in cancer and apoptotic pathways (Supplementary Table 3). [score:3]
It has been shown to target BCL2L1 and TP53, in consequence cancer cell proliferation was decreased with increased doses of miR-491-5p. [score:3]
Our results show that only miR-491-5p significantly regulates PRINS. [score:2]
However, specific knockdown of PRINS had no effects on miR-491-5p levels. [score:2]
[37] In pancreatic cancer, miR-491-5p expression was decreased compared with normal tissue. [score:2]
To determine whether miR-491-5p regulation of PRINS had feedback effects on PI3K/AKT signalling, we examined activation states of downstream kinases after RNAi (siPRINS and miR-491 mimic). [score:2]
Significant knockdown of PRINS in HT-29/B6/TFF3 (P<0.001) did not affect cellular miR-491-5p levels (Supplementary Figures 4a and b). [score:2]
miR-491-5p -mediated regulation of PRINS depends on PI3K/AKT. [score:2]
MiR-491-5p has been reported to efficiently induce apoptosis in ovarian carcinoma by targeting BCL2L1 and accumulating BCL2L11 in its dephosphorylated form. [score:2]
miR-491-5p regulates cellular availability of the lncRNA PRINS. [score:2]
Small interfering RNA (siRNA) against PRINS (siPRINS) was used to determine if PRINS has feedback regulatory effects on miR-491-5p. [score:2]
Transfection of HT-29/B6/TFF3 cells with miR-491-5p mimic compensated for BCL2, BBC3, PLCG2 and PMAIP1 dysregulation (Figure 4b). [score:2]
In general, cell indices of TFF3 -overexpressing clones decreased after siPRINS and even more after miR-491-5p transfection compared with nonsense -transfected controls (Figure 2d). [score:2]
[31] As shown in Figure 1e, three miR-491-5p binding sites together with two miR-329 sites and one miR-326 site were predicted (Supplementary Figure 2). [score:1]
[32] Consequently, we screened for protein-coding transcripts that are relevant to apoptotic signalling [33] and are compensated upon restoring miR-491-5p deficiency, as well as PRINS excess. [score:1]
Exposure of HT-29/B6/mock to IFN- γ/TNF- α caused more than threefold, and significant (P<0.01) increase of apoptotic cells independent of treatment with nonsense, miR-491 or siPRINS (Figures 2a and b, Supplementary Figure 5). [score:1]
TFF3 -dependent decrease of miR-491-5p confers PRINS -mediated resistance to apoptosis. [score:1]
Only co-transfection of the reporter plasmid containing binding site #3 and miR-491-5p mimic resulted in a significantly decreased luciferase activity (P<0.01) and a reporter plasmid including the mutated site proved the specificity of studied interaction (Figure 1g and Supplementary Figure 3). [score:1]
Next, we asked if decreased miR-491-5p and consequently increased PRINS levels are the reason for protective effects of TFF3 against IFN- γ/TNF- α -induced apoptosis in HT-29/B6. [score:1]
[4] In miR-491-5p mimics- as well as siPRINS-experiments, we showed that HT-29/B6/TFF3 cells became more susceptible to apoptosis. [score:1]
As miR-491-5p has been reported to be a pro-apoptotic molecule, 37, 38 we assumed that protective effects of TFF3 rely on miR-491-5p -dependent accumulation of PRINS. [score:1]
Splicing variants and alternative tertiary structures of PRINS may appear in a differentiation -dependent manner, which could be under the control of miRNAs other than miR-491-5p. [score:1]
Cytokine stimulation influenced the observed miR-491-5p-PRINS axis. [score:1]
Cellular PRINS levels were significantly decreased (P<0.05) only after miR-491-5p transfection (Figure 1f). [score:1]
Interestingly, 3 h after cytokine stimulation miR-491-5p tended to be increased in HT-29/B6/TFF3 cells. [score:1]
We conducted gain-of-function experiment using miR-491-5p mimics and loss-of-function experiments using siPRINS. [score:1]
But miR-491-5p transfection, as well as siPRINS along with IFN- γ/TNF- α stimulation caused a marked increase (>6-fold, P<0.0001) of apoptotic cells (Figures 2a and c). [score:1]
Mocks either transfected with miR-491-5p or siPRINS exhibited a significant increase (P [miR-491]<0.05 and P [siPRINS]<0.01) of apoptotic cells (Figures 2a and b, Supplementary Figure 5). [score:1]
Thereby identified PLCG2 and PMAIP1 are apparently controlled by the examined miR-491-5p-PRINS axis. [score:1]
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[+] score: 49
These results suggest that endogenous miR-138, miR-342, miR-491, and miR-541 inhibit telomerase activity and their downregulation during tumorigenesis can results in activation of telomerase. [score:6]
miRNAs miR-133a, miR-138, and miR-491, which specifically inhibited reporter activity, also directly inhibit telomerase activity in cells a few hours after treatment. [score:6]
To address the significance of regulation of telomerase activity by endogenous miRNAs we electroporated inhibitors of miR-138, miR-342, miR-491, and miR-541 into Jurkat cells in which these miRNAs are expressed [42]. [score:6]
Interestingly, the combination of miR-491, miR-541, and miR-342 (MIX1) inhibited telomerase activity more efficiently than any of these miRNAs alone. [score:3]
Our report confirms this finding and demonstrates that at least five additional miRNAs (let-7g*, miR-133a, miR-342-5p, miR-491-5p, and miR-541-3p) directly regulate hTERT. [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]
miR-491-5p induces apoptosis in colorectal cancer cells by binding BCL2L1 (Bcl-X [L]) and inhibits cellular invasion of glioma cells [74], [75]. [score:3]
The luciferase activity of the WT reporter construct was significantly inhibited in cells transfected with precursors of let-7g*, miR-133a, miR-138, miR-342, miR-491, and miR-541 relative to cells transfected with the negative 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]
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]
Both miR-491-5p and miR-541 also inhibit androgen -induced proliferation of prostate cancer cells [77]. [score:3]
The inhibitory effect observed for miR-133a, miR-342, miR-491 and miR-541, was completely or almost completely eliminated when the luciferase assays employed the hTERT 3′UTR constructs with mutated binding sites. [score:2]
The mixtures of miRNAs as well as scrambled control (SC) were always at a concentration of 60 nM; MIX1 (miR-491, miR-541, and miR-342), MIX2 (let-7g*, miR-133a, and, miR-138), MIX3 (MIX1+MIX2). [score:1]
The first combination contained three miRNAs (miR-491, miR-541, and miR-342) that have predicted binding sites in both the 3′UTR of hTERT and in the 3′UTRs of the TCF7, MSI1 and PAX5 genes (Figure 1) (MIX1). [score:1]
Further, the transfection of four of these six miRNAs (let-7g*, miR-133a, miR-138, miR-491) also decreased telomerase activity. [score:1]
Overall, miR-342, miR-491, and miR-541 demonstrated the greatest effect on all three reporters which is consistent since the 3′UTR of these genes have multiple predicted binding sites for the miRNAs examined. [score:1]
miRNAs let-7g* and miR-491 also repeatedly reduced telomerase activity even though this effect was not statistically significant. [score:1]
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[+] score: 32
miRNA Tissue type Mode of action Reference miR-491-5p Cervical cancerUnknown, inhibits hTERT Zhao et al., 2015 miR-1182 Gastric cancerBinds the ORF of hTERT mRNA, preventing translation Zhang et al., 2015 miR-1207-5p Gastric cancerRepresses hTERT in normal tissues Chen et al., 2014 miR-1266 Gastric cancerRepresses hTERT in normal tissues Chen et al., 2014 miR-138 Anaplastic thyroid carcinoma (ATC)Interaction with 3′UTR of hTERT to reduce protein expression Mitomo et al., 2008 let-7g Pulmonary fibrosisInteraction with 3′UTR of hTERT to reduce expression Singh et al., 2010 miR-133a Jurkat cellsInteraction with 3′UTR of hTERT to reduce expression Hrdličková et al., 2014 miR-342 Jurkat cellsInteraction with the 3′UTR of hTERT to reduce expression Hrdličková et al., 2014 miR-541 Jurkat cellsInteraction with the 3′UTR of hTERT to reduce expression Hrdličková et al., 2014 Non-coding RNAs can also target transcription factors involved in the control of hTERT. [score:17]
It is down-regulated in cervical cancer, and enforced expression of miR-491-5p significantly inhibited proliferation through targeting hTERT (Zhao et al., 2015). [score:10]
MicroRNA-491-5p suppresses cervical cancer cell growth by targeting hTERT. [score:4]
The miRNA profile is different for each cell type, but miR-491-5p has been shown to be involved in the initiation and progression of multiple tumor types, including cervical cancer. [score:1]
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[+] score: 25
Following FDR statistical correction for multiple tests, Hsa-miR-491-3P and Hsa-miR 185* were found to be significantly differentially expressed and upregulated: (P [nominal]:9.10 [−5] and 1.8.10 [−4] respectively; FDR-corrected p = 0.031 for both) Figure 1B. [score:6]
MicroRNAs Hsa-miR-185* and Hsa-miR-491-3p were upregulated in suicide completers with low expression of TrkB. [score:6]
Given that suicide completers were selected on the basis of low TrkB-T1 expression, it follows that Hsa-miR-491-3P and/or Hsa-miR 185* could affect the expression of TrkB-T1. [score:5]
B: MicroRNAs differentially expressed after correction for multiple testing (FDR : 0.05) C: Quantification of Hsa-miR-491-3P in the microarray samples by real time PCR. [score:3]
RT-PCR investigation of Hsa-miR-185* expression in frontal cortex samples of cases and controls included in the initial array study showed a positive correlation (R [2] = 0.6638 p = 0.014) with array results and validated a significant) increase of this microRNA among suicides (Figure 1D, t = 2.861, df = 6, p = 0.028), while the differential expression of Hsa-miR-491-3P was not validated by RT-PCR (Figure 1C, t = 0.9476, df = 6, p = 0.379). [score:3]
Hsa-miR-185* and Hsa-miR-491-3P are indicated by a red square. [score:1]
Bioinformatic analyses revealed five putative binding sites for the DiGeorge syndrome linked microRNA Hsa-miR-185*in the 3′UTR of TrkB-T1, but none for Hsa-miR-491-3P. [score:1]
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[+] score: 25
While expression of some of these miRNAs seemed to be specifically dysregulated in certain tumor stages, 12 miRNAs, including 4 up-regulated (miR-200c, miR-487a, miR-491-3p and miR-452) and 8 down-regulated miRNAs (miR-125b, miR-142-3p, miR-199a-5p, miR-22, miR-299-3p, miR-29a, miR-429, and miR-532-5p), were identified to be commonly dysregulated in all ccRCC tumors at different stages (Table 1). [score:11]
Eleven commonly dysregulated miRNAs, including 3 up-regulated (miR-487a, miR-491-3p and miR-452) and 8 down-regulated (miR-125b, miR-142-3p, miR-199a-5p, miR-22, miR-299-3p, miR-29a, miR-429, and miR-532-5p), were identified in ccRCC tumor samples as compared with adjacent nontumorous samples. [score:7]
Eleven miRNAs were identified to be commonly dysregulated, including three up-regulated (miR-487a, miR-491-3p and miR-452) and eight down-regulated (miR-125b, miR-142-3p, miR-199a-5p, miR-22, miR-299-3p, miR-29a, miR-429, and miR-532-5p) in tumor tissues as compared with adjacent normal tissues. [score:7]
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[+] score: 23
The expression of miR-410 was significantly up-regulated (p < 0.05), miR-491 displayed no expression change, miR-384 and miR-506 were both down-regulated respectively (p < 0.05) in A549 cells (Figure 1B). [score:11]
B. The expression of miR-410, miR-491-5P, miR-384 and miR-506-3P in A549 cells was determined by qRT-PCR. [score:3]
Figure 1 A. Four miRNAs (miR-410, miR-491-5P, miR-384 and miR-506-3P) were predicted by both algorithms (TargetScan, miRanda). [score:3]
A. Four miRNAs (miR-410, miR-491-5P, miR-384 and miR-506-3P) were predicted by both algorithms (TargetScan, miRanda). [score:3]
22 miRNAs were preliminarily filtered (data not shown) and then four of them (miR-410, miR-506, miR-491, miR-384) were selected because of their lower free binding energy which meant more possibility that miRNA might bind to its target gene (Figure 1A). [score:3]
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[+] score: 21
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-188, 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-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
Among the downregulated miRNAs; miR-29 was found to target DNMT1, DNMT3A, DNMT3B and HDAC4),while miR-30 targets DNMT3A, HDAC2, HDAC3, HDAC6 and HDAC10, miR-379 targets DNMT1 and HDAC3 and miR-491 (miR-491 targets DNMT3B and HDAC7. [score:12]
Out of these 25 miRNAs, 18 miRNAs were differentially expressed in a consistent manner between the 2 groups (Figure 4A, highlighted); 8 miRNAs were downregulated in both groups (miR-16, miR-200, miR-205, miR-3064, miR-379, miR-431, miR-485 and miR-491) and 10 miRNAs were upregulated in both groups (miR-194, miR-1894, miR-211, miR-3072, miR- 3077, miR-4436, miR-5128, miR-669a, miR-669c and miR-6967). [score:9]
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[+] score: 20
Real-time PCR confirmed microarray analysis results: expression of miR-302a and miR-491-3p was up-regulated (Fig. 2) and miR-520d-3p and miR-383 was down-regulated (Fig. 2) in patients with NOA. [score:9]
Quantitative real-time PCR analysis confirmed microarray data: miR-302a and miR-491-3p was up-regulated and miR-520d-3p and miR-383 was downregulated in NOA patients. [score:7]
For example, one of the predicted target genes of miR-302a and miR-383 is MLH1, while miR-491-3p and miR-520d-3p is SCP1 and SCP3, respectively. [score:3]
To confirm the results obtained by microarray analysis, quantitative real-time RT-PCR analysis of normal and NOA testicular samples was performed for miR-302a, miR-491-3p, miR-520d-3p and miR-383. [score:1]
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[+] score: 20
[36– 38] miR-125b TLR signaling Abolish the cytokine production[39] miR-19a Enhance IFNα and interleukin-6[42] miR-192Upregulate TGF-β1 expressionMediate HCV infection -associated fibrogenesis[44] miR-152Target the WNT1 3′-UTRRegulate proliferation, G1-S transition, and colony formation in HepG2 cells[45] miR-491 Enhance HCV replication[46] miR-449a NOTCH signaling Inhibit TNFa -mediated activation of YKL40[49] HCV hepatitis C virus IFN interferon miRNA microRNAs DUSP dual specific phosphatases TLR toll-like receptor JAK/STAT Janus kinase/signal transducer and activator of transcriptions SOCS suppressors of cytokine signaling TGF-β transforming-growth factor-β PI3K/Akt phosphatidylinositol 3-kinase and Akt/protein kinase B NS5A non-structural protein 5A HZ made contributions to conception and design of the work, and was a major contributor in writing the manuscript. [score:13]
miR-491, identified to be downregulated by HCV infection in Huh7 cell line, can enhance HCV replication both in HCV replicon cells and in cell culture-infectious HCV-infected cells. [score:4]
The study finds that the effect of miR-491 on HCV replication can be abolished by inhibiting PI3K, which indicates that augmentation of HCV replication by miR-491 is dependent on the PI3K/Akt pathway [46]. [score:3]
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[+] score: 20
MMP9 (a gelatinase that binds and degrades gelatin) is a direct target of miR-491-5p and miR-211-5p, which are both upregulated in tumor samples [35, 78, 79], and MMP3 (an archetypal metalloproteinase with stromelysin activity) is targeted by miR-152-3p [80]. [score:9]
miR-124-3p is reported to radiosensitize human glioma cells by downregulating CDK4 [71], while CDK6 is a direct target of miR-138-5p and miR-491-3p/5p [35, 72]. [score:7]
miR-7-5p [33], miR-128-3p [34], miR-491-5p [35] and miR-218-5p [36] coordinately regulate the expression of EGFR in human GBM. [score:4]
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[+] score: 19
Among these 11 miRNAs, only miR-491-3p was significantly downregulated, while the others were prominently upregulated. [score:7]
miR-2136, let-7f-5p, miR-431-5p, and miR-491-3p were upregulated in both 3-month-old and 6-month-old AD mice, implying their role in the development of AD. [score:5]
Considering a probe signal of over 100 as abundance, eleven of the 28 miRNAs (miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p) were shown to have targets that are tightly related to AD and could easily be detected. [score:3]
Furthermore, levels of miR-2136, let-7f-5p, miR-431-5p, and miR-491-3p were higher in both 3-month-old and 6-month-old APP/PS1 mouse brain, indicating their potential involvement in the progression of AD (Figure 2). [score:1]
miR-491 plays a role in different types of cancers, such as glioblastoma and tongue cancer [40, 41]. [score:1]
To our knowledge, this is the first study to identify the potential effects of miR-342-3p, miR-491-3p, miR-539-3p, miR-376c-3p, miR-10a-5p, and miR-652-5p in the progression of AD. [score:1]
For further analysis, we chose 11 evidently different miRNAs that were conserved between both human and mouse: miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p. [score:1]
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[+] score: 18
Other miRNAs from this paper: hsa-mir-134, hsa-mir-149, hsa-mir-130b, hsa-mir-146b, hsa-mir-181d
Among them 35 miRNAs are significantly (p ≤ 0.05) down-regulated and only one miRNA (miR-491) is up-regulated in SCC084/R cells. [score:7]
However, miR-491-5p displayed a significantly low level of expression in pancreatic cancer cell and mediated cell apoptosis by targeting both Bcl-xL and TP53 53. [score:5]
In consistent with our results, a report also suggested that the level of miR-491-5p expression correlated inversely with GIT1, which in turn is correlated with lymph node metastasis and tumour grade in OSCC clinical samples and finally they suggested miR-491-5p and GIT1 as biomarkers for prognosis in this cancer 54. [score:3]
Finally, we have established 6 miRNA signatures (miR-130b, miR-134, miR-149, miR-491, miR-181d, miR-146b) which are significantly (p ≤ 0.05) differentially expressed and common in both the cisplatin resistant cell lines (SCC084/R and SCC131/R) compared to their parental cell lines (SCC084 and SCC131) (Fig. 7C and). [score:2]
There are 6 miRNAs, miR-130b, miR-134, miR-149, miR-491, miR-181d, miR-146b, which are common in both the resistant cells. [score:1]
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[+] score: 16
In OSCC (oral squamous cell carcinoma), Huang et al. showed that miR-491-5p inhibited migration/invasion and metastasis of oral cancer cells and this was also through targeting GIT1 expression. [score:7]
GIT1 could be directly targeted by miR-149 and miR-491-5p in the different context of cancer cells [91, 92]. [score:4]
Thus, miR-149 and miR-491-5p are potent metastasis suppressors in breast and oral cancer respectively. [score:3]
In OSCC, tumors with low levels of miR-491-5p have a higher tendency to form lymph node metastasis [92]. [score:1]
Moreover, low level of miR-491-5p and high level of GIT1 were correlated with lymph node metastasis and overall survival of OSCC patients [92]. [score:1]
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[+] score: 15
There were no microRNAs regulated after 1 hour in culture, however after 4 hours in culture miR-491-3p, miR-34b, miR-595, miR-328 miR-1281 and miR-483-3p were significantly upregulated, with none being downregulated. [score:8]
However, after 4 hours in culture, significant upregulation was seen for miR-491-3p, miR-34b, miR-595, miR-328, miR-1281 and miR-483-3p, with no microRNAs being significantly downregulated. [score:7]
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[+] score: 12
Furthermore, miR-491-5p was shown to suppress invasion and metastatic potential of OSCC cells in vitro and in vivo by targeting the expression of G-protein-coupled receptor kinase-interacting protein 1 (GIT1), which further regulated the expression of focal adhesions, steady-state levels of paxillin, phospho-paxillin, phospho-FAK, EGF/EGFR -mediated extracellular signal-regulated kinase (ERK1/2) activation, and MMP2/9 levels and activities [59]. [score:11]
miR-31, miR-17/20a, miR-125b, miR-155, miR-181, miR-375 and miR-491-5p, miR-205, and miR-let7d were found to be associated with lymph node metastasis and poor OSCC patient survival [38, 59, 60, 65, 72, 77– 80]. [score:1]
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[+] score: 11
The expression profile of infected and uninfected cells was evaluated using a miRNA microarray, and 16 miRNAs were reported to be up-regulated (miR-4290, miR-4279, miR-625*, miR-let-7e, miR-1290, miR-33a, miR-3686, miR-378, miR-1246, miR-767-5p, miR-320c, miR-720, miR-491-3p, miR-3647, miR-451 and miR-4286) and 4 down-regulated (miR-106b, miR-20a, miR-30b and miR-3653) during dengue infection. [score:7]
This result is consistent with available data on some of the targets of altered miRNAs, such as miR-1204, which is related to cell death induction, miR-491-5p, which is a negative regulator of p53 and Bcl-XL, and miR-512-5p, which represses nucleotide -binding oligomerization domain containing 2 (NOD2). [score:4]
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[+] score: 11
Additionally, 9 miRNAs (hsa-miR-484, hsa-miR-499-5p, hsa-miR-126*, hsa-miR-491-5p, hsa-miR-1303, hsa-miR-539, hsa-miR-25*, hsa-let-7e*, and hsa-miR-194*) were upregulated in 10 diseases while not downregulated in any other, as the balloon plot (Figure  3) of all miRNAs significant in at least 8 of 19 diseases (>40%) shows. [score:11]
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[+] score: 11
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-296, 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-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
Acute liver injury upregulates microRNA-491-5p in mice, and its overexpression sensitizes Hep G2 cells for tumour necrosis factor-alpha -induced apoptosis. [score:6]
Stimulation of HCC proliferationBudhu et al., 2008; Gramantieri et al., 2008; Huang et al., 2009, 2011 miR-373 Invasion and metastasisMeng et al., 2007; Bartels and Tsongalis, 2009; Wu et al., 2011 miR-374 DevelopmentWang et al., 2008; Wong et al., 2008, 2010; Koh et al., 2013 miR-375 Stimulation of HCC proliferationLiu et al., 2010; He et al., 2012 miR-376a Proliferation and apoptosisMeng et al., 2007; Zheng et al., 2012b miR-423 Enhanced CDK2 activityLin et al., 2011 miR-491-5p Inhibition of TNF-α-related apoptosisYoon et al., 2010 miR-500 Elevated in HCC, returned to physiologic level after surgical interventionYamamoto et al., 2009 miR-637 Active STAT3Zhang et al., 2011 let-7a/a-1/a-2/b/c/d/e/f/f-2/g Development. [score:5]
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[+] 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-20a, hsa-mir-21, hsa-mir-28, hsa-mir-29a, hsa-mir-93, hsa-mir-100, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-34a, hsa-mir-181c, hsa-mir-182, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-210, hsa-mir-217, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-141, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-134, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-106b, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-372, hsa-mir-382, hsa-mir-148b, hsa-mir-196b, hsa-mir-424, hsa-mir-448, hsa-mir-449a, hsa-mir-483, hsa-mir-501, hsa-mir-503, 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-320c-1, 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, hsa-mir-320c-2, hsa-mir-548q, hsa-mir-548s, 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-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
Similarly, up-regulation of miR-155 and miR-141, as well as down-regulation of miR-152 and miR-491 (which are tumor suppressors), promotes hepatocellular carcinoma in HCV infection [43, 65]. [score:9]
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[+] score: 9
This effect was due to direct targeting of EGFR by miR-491-5p and consequent inhibition of downstream AKT and RAS-MAPK signaling pathways. [score:6]
Induction of apoptosis by miR-491-5p in the IGROV1-R10 cell line was mimicked by a combination of EGFR inhibition together with a BIM -mimetic molecule. [score:3]
[1 to 20 of 2 sentences]
[+] score: 8
Several cellular miRNAs, such as miR-323, miR-491, miR-654, and Let-7c have recently been reported to inhibit H1N1 influenza A virus replication by downregulating the viral gene expression in infected MDCK or A549 cells [19, 20]. [score:8]
[1 to 20 of 1 sentences]
[+] score: 7
A spectrum of miRNAs including miR-337-5p, miR-17-1, miR-15a, miR-491-5p, miR-339, miR-337-3p, miR-241, miR-19a were predicted to down regulate oncogenic targets like TGFβ, BCLXW, BCL-Xl, STATs, c-MYC and SMAD (as represented by red lines). [score:4]
For example, miR-337-5p, miR-17-1, miR-15a, miR-491-5p, miR-339, miR-337-3p, miR-241, miR-19a were found to modulate oncogenic targets including TGFβ, STATs, c-MYC and SMAD. [score:3]
[1 to 20 of 2 sentences]
[+] score: 7
The top 20 miRNAs significantly up- or down-regulated in Exo [Hypoxic] compared to Exo [Normoxic] are listed in Table 1. Nine miRNAs were expressed at a significantly lower level in Exo [Hypoxic] compared to Exo [Normoxic]: miR-521 (Fold change = 0.0005), miR-27a (Fold change = 0.24), miR-324 (Fold change = 0.446), miR-579 (Fold change = 0.448), miR-502 (Fold change = 0.396), miR-222 (Fold change = 0.232), miR-135b (Fold change = 0.325), miR-146a (Fold change = 0.456) and miR-491(Fold change = 0.482). [score:4]
Among these, 15 miRNAs (miR-143, miR-146a, miR-181a, miR-204, miR-222, miR-27a, miR-335, miR-433, miR-491, miR-502, miR-521, miR-92a, miR-127, miR-135b and miR-451) target 211 mRNAs when the confidence limit was set as “Experimentally Observed” only. [score:3]
[1 to 20 of 2 sentences]
[+] score: 7
Five poorly conserved miRNAs namely; miR-129, miR-491, miR-4795, miR-561, and miR-4717 have been predicted to target the 3′UTR region surrounding the ABCB1 4036A> G SNP using the TargetScanHuman 6.1 miRNA target prediction software. [score:7]
[1 to 20 of 1 sentences]
[+] score: 7
We examined the expression of the ten most over- (miR-192-5p, 103a-5p, 145-5p, -215, -451a, -23b-3p, -21-5p, 23a-3p, 24-3p, 191-5p) and under- expressed (miR-491-3p, -574, -18a, -488-5p, -216a, -548, -520d, -20b, -218, -346) human BE miRNA in three BE cell lines, BAR-T, CP-A and CP-C. The mean number of reads by NGS for the ten most expressed miRNA in human BE specimens was 78178 (range 27,374–240,611). [score:7]
[1 to 20 of 1 sentences]
[+] score: 7
For example, in multi-drug resistant tongue cancer, miR-491-3p, which regulates Rictor expression is downregulated, leading to decreased mTORC2 activity and phosphorylation of the hydrophobic motif of SGK1 [87]. [score:7]
[1 to 20 of 1 sentences]
[+] score: 6
Recent studies demonstrated that miR-138, miR-133a, miR-342, miR-491-5p, miR-541, miR-1207-5p, miR-1266 and miR-1182 control hTERT expression in leukemic T-cell lymphoblasts, gastric cancer, cervical cancer, thyroid carcinoma and head and neck squamous cell carcinoma [28– 31, 33]. [score:3]
Recent studies reported a role of miR-133a, miR-138, miR-541, miR-491-5p, miR-512-5p, miR-1182, miR-1207-5p and miR-1266 in the control of hTERT expression in various types of cancer cells [27– 33]. [score:3]
[1 to 20 of 2 sentences]
[+] score: 6
Additionally, let-7g*, miR-133a, miR-342-5p and miR-491-5p downregulate telomerase activity and inhibit cell proliferation [169]. [score:6]
[1 to 20 of 1 sentences]
[+] score: 6
Simultaneously, miRNA-149, miRNA-638, and miRNA-491 were up-regulated due to HCV infection and enhance the viral replication by inhibiting the AKT/PI3 kinase (Conrad and Niepmann, 2014). [score:6]
[1 to 20 of 1 sentences]
[+] score: 6
For example, a few miRNAs, such as let-7c, miR-2911, miR-323, miR-491, and miR-654 had been found to inhibit IAV replication by directly targeting viral genes (Song et al., 2010; Ma et al., 2012; Zhou et al., 2015). [score:6]
[1 to 20 of 1 sentences]
[+] score: 6
The third key factor, hsa-mir-491, was not identified, but Shi et al. [74] found that hsa-mir-491 is down-regulated in gastric cancer patients and has an inhibitory effect on cell proliferation. [score:6]
[1 to 20 of 1 sentences]
[+] score: 6
Five out of the ten most deregulated miRNAs (miRNAs hsa-miR-664, hsa-miR-422a, hsa-miR-584, hsa-miR-1275, and hsa-miR-491-5p) have not yet been associated with any specific functions or human diseases. [score:4]
The ten miRNAs that were most significantly deregulated included hsa-miR-145 (1.46·10 [−7]), hsa-miR-186 (2.89·10 [−7]), hsa-miR-664 (5.25·10 [−5]), hsa-miR-20b (1.48·10 [−4]), hsa-miR-422a (1.48·10 [−4]), hsa-miR-142-3p (1.54·10 [−4]), hsa-miR-584 (1.56·10 [−4]), hsa-miR-223 (1.63·10 [−4]), hsa-miR-1275 (1.16·10 [−4]) and hsa-miR-491-5p (2.83·10 [−4]). [score:2]
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[+] score: 6
[89] Denoyelle et al. [90] found that miR-491-5p efficiently induces apoptosis in ovarian cancer cells by directly inhibiting Bcl-xL expression and by inducing Bim accumulation. [score:6]
[1 to 20 of 1 sentences]
[+] score: 6
We did note that BCL2 had seed-region matches with all of these miRNAs except miR-491, suggesting that associations likely exist but were not detected in this study, possibly because of an effect on protein level rather than on mRNA expression. [score:3]
BLC2 has been examined with several targeted miRNAs, including miR-491, miR-143, miR-148a, miR-365, miR-1915, miR-204, and miR-125b [4– 6, 8, 29– 31]. [score:3]
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[+] score: 5
Name Predicted targets 1 miR-1260b DNMT3A, HOXD1, OCT1, FGF12, GDF11 2 miR-720 DNMT3A, NANOG 3 miR-1280 JAG2, ZNF544, UBTF 4 miR-491-3p EGFR, SOX-11, COL12A1, NOV/CCN3 5 miR-1260a DNMT3A, PDGFD, HOXD1, SEMA3A, FGF12 6 miR-138-1 TIEG2, JMJD1C, CYCLIN D3, ROCK2, PPARδ Table shows the selected possible mRNA targets related to stemness and cell differentiation. [score:5]
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[+] 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-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-98, hsa-mir-99a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-30b, hsa-mir-130a, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-185, hsa-mir-193a, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-181b-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-363, hsa-mir-374a, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-423, hsa-mir-20b, hsa-mir-193b, hsa-mir-181d, hsa-mir-92b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, bta-mir-29a, bta-let-7f-2, bta-mir-148a, bta-mir-18a, bta-mir-20a, bta-mir-221, bta-mir-27a, bta-mir-30d, bta-mir-320a-2, bta-mir-99a, bta-mir-181a-2, bta-mir-27b, bta-mir-30b, bta-mir-106a, bta-mir-10a, bta-mir-15b, bta-mir-181b-2, bta-mir-193a, bta-mir-20b, bta-mir-30e, bta-mir-92a-2, bta-mir-98, bta-let-7d, bta-mir-148b, bta-mir-17, bta-mir-181c, bta-mir-191, bta-mir-200c, bta-mir-22, bta-mir-29b-2, bta-mir-29c, bta-mir-423, bta-let-7g, bta-mir-10b, bta-mir-24-2, bta-mir-30a, bta-let-7a-1, bta-let-7f-1, bta-mir-30c, bta-let-7i, bta-mir-25, bta-mir-363, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-15a, bta-mir-19a, bta-mir-19b, bta-mir-331, bta-mir-374a, bta-mir-99b, hsa-mir-374b, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, bta-mir-1-2, bta-mir-1-1, bta-mir-130a, bta-mir-130b, bta-mir-152, bta-mir-181d, bta-mir-182, bta-mir-185, bta-mir-24-1, bta-mir-193b, bta-mir-29d, bta-mir-30f, bta-mir-339a, bta-mir-374b, bta-mir-375, bta-mir-378-1, bta-mir-491, bta-mir-92a-1, bta-mir-92b, bta-mir-9-1, bta-mir-9-2, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, bta-mir-181b-1, bta-mir-320b, bta-mir-339b, bta-mir-19b-2, bta-mir-320a-1, bta-mir-193a-2, bta-mir-378-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, bta-mir-148c, hsa-mir-374c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-378j, bta-mir-378b, bta-mir-378c, bta-mir-378d, bta-mir-374c, bta-mir-148d
In addition, many miRNA families showed low expression (count number <100) in milk exosomes, such as the miR-1, miR-130, miR-17, miR-10, miR-29, miR-374, mir-9, miR-15 and miR-491 families (Figure 12F), which are routinely expressed in specific tissues [53– 56]. [score:5]
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[+] score: 5
In 2010, Song’s group reported that miR-323, miR-491 and miR-654 could target the viral PB1 gene [34]. [score:3]
As miR-491 had been verified to target viral PB1 of A/WSN/33 [34], and the binding sites were conserved with that of the ssc-miR-491 in viral PB1 of SIV-H1N1/2009, the pair of ssc-miR-491 and PB1 was considered as the positive control. [score:2]
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[+] score: 4
Zhao Q. Zhai Y. X. Liu H. Q. Shi Y. A. Li X. B. MicroRNA-491-5p suppresses cervical cancer cell growth by targeting hTERTOncol. [score:4]
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[+] score: 4
Specifically, miR-27b, miR103, miR107 were previously reported to play key roles in regulating CYP3A and CYP2C 20 33, while miR-142 and miR-491 were reported to play key roles in regulating phase II enzymes, namely UGT1A1 and UGT1A3 34 35. [score:3]
Therefore, a total of 13miRNAs, namely miR-21-5p, miR-27a-3p, miR-27b-3p, miR-103a-3p, miR-106a-5p, miR-107, miR-126-5p, miR-130a-3p, miR-142-5p, miR-206, miR-371b-5p, miR-491-3p, and miR-1260b, were selected. [score:1]
[1 to 20 of 2 sentences]
[+] score: 4
Other miRNAs from this paper: hsa-mir-1260b
MicroRNA-491-5p suppresses cervical cancer cell growth by targeting hTERT. [score:4]
[1 to 20 of 1 sentences]
[+] score: 4
Although Ishida et al. [30] revealed that miR-491 regulates HCV replication, the miRNAs associated with HCV entry were not completely identified. [score:2]
Previous studies revealed that several miRNAs such as let-7b [24], miR-27a [25], miR-122 [26], miR-155 [27], miR-196 [28], miR-199a [29], and miR-491 [30] regulate HCV replication. [score:2]
[1 to 20 of 2 sentences]
[+] score: 4
Futher, hsa-mir-491, which is involved in neurosteroidogenesis and pathogenesis of multiple sclerosis [15], was found significantly downregulated by PQ. [score:4]
[1 to 20 of 1 sentences]
[+] score: 3
Recently, many antiviral miRNAs (miR-323, miR-491, miR-654, and Let-7c) have been found to reduce IAV replication by targeting the viral genome 10 11. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
It also has been shown that cellular miR-323, miR-491, and miR-654 could inhibit replication of the H1N1 influenza A virus through binding to the PB1 gene [6]. [score:3]
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[+] score: 3
Influenza virus infection modulates multiple cellular miRNAs, and miR-323, miR-491, and miR-654 have been shown to inhibit viral replication by binding to the viral PB1 gene [48], while miR-507 and miR-136 have potential binding sites within the viral PB2 and HA genes [49]. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
In another report, results showed that miR-323, miR-491 and miR-654 could inhibit replication of H1N1 influenza A virus through binding to the conserved region of the PB1 gene [16]. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
Moreover, several studies have demonstrated that cellular microRNAs (miR-323, miR-491, miR654, miR-146a) inhibit influenza virus replication or propagation [23, 24]. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
Other miRNAs from this paper: hsa-mir-125b-1, hsa-mir-125b-2
mir-491 is predicted to regulate BCL2L1 in the current analysis. [score:2]
The mature products of mir-491 (miR-491-5p and miR-491-3p) have been reported to possess different functions in different cancers [34– 36]. [score:1]
[1 to 20 of 2 sentences]
[+] score: 3
Song et al. screened host miRNAs and found that miR-323, miR-491 and miR-654 inhibit the replication of the H1N1 IAV in MDCK cells by binding to the 3′ coding region rather than the 3′-UTR of the PB1 gene. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
Origin Tongue Gingiva Tongue [8], [9], [10], [26] HPV status HPV-16 − − − [27] HPV-18 − − + [27] Basal invasive capacity + ++ +++ [9], [28], [29] Genetic background TP53 + + WT [30], [31] CDKN2A (p16) + + + [30], [32], [33] Critical proteins LOX ++ ++ + [9] Tid1 + + − [10] CK1ε ++ + N/A [29] SIRT1 + + N/A [26] Tumor suppressor miRNAs miR-10b +++ + + [27] miR-196a +++ + + [27] miR-491-5p + ++ ++ [34] miR-410 + + N/A [35] miR-99a + + N/A [35] miR-21 + N/A N/A [35] Oncogenic miRNA miR-31 N/A + + [35] miR-146a N/A + + [36] miR-187 N/A + + [37] WT: wild type; N/A: not available. [score:3]
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[+] score: 3
During moderate PH, miR-21, miR-23b, miR-130a, miR-491 and miR-1246 are moderately upregulated but, are more pronounced in severe PH, compared to the controls. [score:3]
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[+] score: 3
Tao K. Yang J. Guo Z. Hu Y. Sheng H. Gao H. Yu H. Prognostic value of miR-221-3p, miR-342-3p and mir-491-5p expression in colon cancerAm. [score:3]
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[+] score: 3
Tao K. Yang J. Guo Z. Hu Y. Sheng H. Gao H. Yu H. Prognostic value of miR-221–3p, miR-342–3p and miR-491–5p expression in colon cancer Am. [score:3]
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[+] score: 2
The miRNAs miR-491-5p, miR-125b, miR-218, miR-224, and miR-338-3p, were reported to regulate MMP9 in various cell types [11]. [score:2]
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[+] score: 2
miR-124 and miR-491-3p were regulated in opposite manners by the IFNs and EV71. [score:2]
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org/), a set of miRNAs were predicted to have potential interaction with circUBAP2, including miR-150, miR-135, miR-101, miR-181, miR-23, miR-149, miR-139, miR-491, miR-124, miR-301m miR-328, miR-122, miR-186, let-7, miR-132, miR-191, miR-425, miR-125, miR-149, miR-143, and miR-146a. [score:1]
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In a small-scale analysis, others found that a group of miRNAs that are altered by hypoxia in trophoblasts (miR-27a, miR-30d, miR-141, miR-200c, miR-424, miR-205 and miR-451, miR-491, miR-517a, miR-518b, miR-518e, and miR-524) is elevated in FGR pregnancies (n = 14 FGR versus n = 14 controls) [47]. [score:1]
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The involvement of microRNAs in major depression, suicidal behavior, and related disorders: a focus on miR-185 and miR-491-3p. [score:1]
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By contrast, 10 of 11 significantly decreased microRNAs got optimal AUC, the AUC of these microRNAs were 0.936, 0.758, 0.946, 0.991, 0.992, 0.970, 0.837, 0.922, 0.838, 0.966 for miR-135b, miR-138-5p, miR-193b-3p, miR-302b-3p, miR-302c-3p, miR-338-3p, miR-491-3P, miR-575, miR-4254 and miR-4643 respectively (Fig. 6). [score:1]
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A previous report discovered that three miRNAs: miR-323, miR-491, and miR-654, were able to decrease H1N1 production in madin darby canine kidney (MDCK) cells via binding to a same conservative site on PB1 mRNA and subsequently inducing mRNA degradation [26]. [score:1]
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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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Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-16-2, hsa-mir-221, hsa-mir-433
These miRNAs include miR-491, miR-433-3p, miR-221, and miR-16 [21– 24]. [score:1]
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In another study, they indicated that the CD44 3′UTR is also the ceRNA for collagen type 1α1 (Col1α1) mediated by hsa-miR-328-5p and the ceRNA for fibronectin type 1 (FN1) mediated by hsa-miR-512-3p, hsa-miR-491-5p, and hsa-miR-671-5p [40]. [score:1]
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They are as follows: let-7a, let-7c, let-7e, let-7f, let-7g, let-7i, miR-15b, miR-16, miR-18a, miR-22, miR-26b, miR-27a, miR-27b, miR-29b, miR-30c, miR-125b, miR-133b, miR-146b, miR-148a, miR-150, miR-155, miR-181a, miR-181b, miR-181d, miR-223, miR-320, miR-491, and miR-494. [score:1]
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Among of them, 12miRNAs (hsa-miR-139-5p, hsa-miR-638, hsa-miR-107, hsa-miR-331-3p, hsa-miR-21-3p, hsa-miR-134-5p, hsa-miR-16-1-3p, hsa-miR-339-5p, hsa-miR-106b-5p, hsa-miR-423-3p, hsa-miR-491-3p, hsa-miR-24-3p) were related to cancers. [score:1]
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org) Rank miRNA 1 miR-377 2 miR-342 3 miR-491 4 let-7i 5 let-7a Bioinformatics analysis of the BCL-xL 3’-UTR using RNAhybrid and miRbase predicted two potential binding sites for miR-377 at positions 1238 and 1412 (Additional file 1: Figure S1A). [score:1]
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Other miRNAs from this paper: hsa-mir-182, hsa-mir-150, hsa-mir-155, hsa-mir-335
We also identified conserved miRNAs that acted to repress cell growth in our screen, including miR-491 and miR-335. [score:1]
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For example, computational analysis indicated that miRNAs that interact with the CD44 3′-UTR also have binding sites in other matrix encoding mRNA 3′-UTRs, including collagen type 1α1 (Col1α1) repressed by miR-328 and fibronectin type 1 (FN1) repressed by miR-512-3p, miR-491 and miR-671 [19]. [score:1]
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