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35 publications mentioning mmu-mir-370

Open access articles that are associated with the species Mus musculus and mention the gene name mir-370. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 422
Induction of miR-370 over -expression attenuated the EGFR expression while inhibition of endogenous miR-370 expression by transfection with miR-370 inhibitor increased the EGFR expression in lung cancer cells. [score:13]
Furthermore, we found that induction of miR-370 over -expression attenuated the EGFR expression and inhibited the proliferation, clonogenicity, and invasion of lung cancer cells while inhibition of endogenous miR-370 by transfection with miR-370 inhibitor significantly enhanced the EGFR expression and the proliferation, clonogenicity, and invasion of lung cancer cells. [score:13]
These data demonstrated that induction of miR-370 expression significantly down-regulated the EGFR expression and inhibited the growth and angiogenesis of xenograft NSCLC tumors in mice. [score:10]
Therefore, induction of miR-370 over -expression inhibited proliferation, clonogenicity, wound healing and invasion while inhibition of endogenous miR-370 by transfection with miR-370 inhibitor enhanced proliferation, clonogenicity, wound healing and invasion of XWLC-05 and H157 cells. [score:9]
MiR-370 over -expression inhibits while inhibition of miR-370 expression enhances the proliferation, colony formation, wound healing and invasion of XWLC-05 and H157 cells. [score:9]
These, together with observation of down-regulated miR-370 expression in most lung cancer cells tested, suggest that miR-370 may inhibit the development and progression of lung cancers. [score:9]
Induction of miR-370 over -expression attenuates the EGFR expression and down-regulates the ERK and AKT signaling in XWLC-05 and H157 cells. [score:8]
We found that miR-370 acted as a tumor suppressor to reduce EGFR expression and inhibited the growth and metastasis of lung cancers by down -regulating the ERK1/2 and AKT signaling. [score:8]
MiR-370 over -expression significantly reduced the EGFR 3′UTR-regulated luciferase activity, suggesting that miR-370 may bind to the 3′UTR of the EGFR to inhibit the EGFR expression in lung cancer cells. [score:8]
In contrast, inhibition of endogenous miR-370 by transfection with miR-370 inhibitor significantly enhanced the proliferation, clonogenicity, wound healing and invasion in XWLC-05 and H157 cells, accompanied by increased levels of EGFR and HIF-1α expression as well as the ERK1/2 and AKT activation. [score:7]
Induction of miR-370 over -expression reduces EGFR and HIF-1α expression and inhibits the ERK and AKT phosphorylation in XWLC-05 and H157 cells. [score:7]
As shown in Figure 3A, induction of miR-370 over -expression dramatically reduced the proliferation rates while induction of miR-370 inhibitor expression enhanced the proliferation rats of XWLC-05 and H157 cells, relative to the control transfected with negative control. [score:7]
More importantly, miR-370 over -expression inhibited the growth, angiogenesis and metastasis of implanted lung tumors in mice, accompanied by attenuating EGFR and Ki67 expression as well as MVD in the tumors. [score:7]
While one study indicates that miR-370 expression is associated with poor prognosis of patients with lung adenocarcinoma [29], another study reveals that induction of miR-370 over -expression inhibits the proliferation and promotes apoptosis of human lung cancer A549 and H358 cells [30]. [score:7]
We found that transfection with miR-370 significantly increased levels of miR-370 expression, but decreased EGFR mRNA transcripts (Figure 2A and 2D) while transfection with miR-370 inhibitor significantly decreased the levels of miR-370 expression, but increased EGFR mRNA transcripts in both XWLC-05 and H157 cells, relative to their controls (Figure 2B and 2E). [score:7]
MiR-370 over -expression inhibits the lung metastasis of xenograft NSCLC tumors in vivoFinally, we examined the effect of miR-370 over -expression on the lung metastasis of xenograft NSCLC tumors in vivo. [score:7]
Our findings extended a previous report that miR-370 inhibits the progression of NSCLC by targeting the TRAF4 [30], but disagreed with a previous report that miR-370 expression is associated with poor prognosis of lung cancers [29]. [score:7]
Previous studies have shown that miR-370 can promote liver cancer cell apoptosis by targeting the AKT signaling and inhibits glioma cell proliferation and bladder cancer metastasis by targeting the β-catenin [38, 41, 42]. [score:7]
The reduced EGFR and Ki67 expression in the implanted tumors further supported that miR-370 over -expression inhibited proliferation of lung cancer cells in vitro. [score:7]
Given that the ERK and AKT signaling are important for the growth, angiogenesis and metastasis of cancers the inhibition of lung cancer growth, metastasis and angiogenesis by miR-370 over -expression may be also mediated by miR-370 attenuating the EGFR expression and down-stream ERK and AKT signaling in vivo. [score:7]
More importantly, miR-370 over -expression inhibited the proliferation, clonogenicity, wound healing and invasion of lung cancer cells in vitro, which were associated with reduced levels of EGFR and HIF-1α expression and the ERK1/2 and AKT activation. [score:7]
Modulation of miR-370 expression alters the neoplastic behaviors of lung cancer XWLC-05 and H157 cells in vitroTo test the function of miR-370 in lung cancer cells, XWLC-05 and H157 cells were transfected with miR-370 mimics, miR-370 inhibitor, control miR-NC or control inhibitor and the dynamic proliferation of different groups of cells was determined by MTT assay. [score:6]
MiR-370 can function as a tumor suppressor by targeting the expression of FoxM1 [25, 26] and TRAF4 [27]. [score:6]
Modulation of miR-370 expression affects the EGFR expression and the EGFR 3′UTR-regulated luciferase activity in lung cancer cells. [score:6]
Recent studies have revealed that miR-370 expression is downregulated in several types of cancer tissues, including bladder cancer [23], neuroblastoma [24], acute myeloid leukemia [25] and others. [score:6]
To determine whether miR-370 regulates the EGFR expression, XWLC-05 and H157 cells were transfected with miR-370 mimics, miR-370 inhibitor, or their corresponding scrambled control. [score:6]
However, miR-370 expression is up-regulated in breast cancer and gastric carcinoma [28]. [score:6]
To explore the molecular mechanisms underlying the action of miR-370, XWLC-05 and H157 cell were transfected with miR-370 mimics, miR-370 inhibitor control miR-NC or control inhibitor. [score:5]
Furthermore, miR-370 over -expression not only attenuated the EGFR and HIF-1α expression, but also significantly reduced the relative levels of ERK1/2 and AKT activation in XWLC-05 and H157 cells. [score:5]
Induction of miR-370 over -expression inhibits the growth and angiogenesis of NSCLC xenograft tumors in vivo. [score:5]
Therefore, induction of miR-370 over -expression inhibited the lung metastasis of xenograft NSCLC tumors in mice. [score:5]
We are interested in further determining whether miR-370 directly binds to the 3′UTR of the EGFR to understand the precise role and mechanisms in regulating the EGFR expression in lung cancer. [score:5]
XWLC-05 and H157 cells were transfected with miR-NC, miR-370 mimics, miR-370 inhibitor NC or miR-370 inhibitor for 24 h. The relative levels of miR-370 and EGFR mRNA transcripts in different groups of cells were determined by quantitative RT-PCR. [score:5]
The levels of miR-370 expression were determined by quantitative RT-PCR and of EGFR expression were determined by Western-blot. [score:5]
In contrast, transfection with miR-370 inhibitor increased the relative levels of EGFR and HIF-1α expression, increased AKT and ERK1/2 phosphorylation in XWLC-05 and H157 cells. [score:5]
Figure 5Induction of miR-370 over -expression inhibits the growth and angiogenesis of NSCLC xenograft tumors in vivoTo establish a subcutaneous tumor mo del in nude mice, XWLC-05 cells were transfected with pre-miR-370 or miR -negative control (miR-NC). [score:5]
These independent experimental results suggest that miR-370 may bind to the 3′UTR of the EGFR mRNA to inhibit EGFR expression. [score:5]
Figure 2XWLC-05 and H157 cells were transfected with miR-NC, miR-370 mimics, miR-370 inhibitor NC or miR-370 inhibitor for 24 h. The relative levels of miR-370 and EGFR mRNA transcripts in different groups of cells were determined by quantitative RT-PCR. [score:5]
Figure 6MiR-370 over -expression inhibits the lung metastasis of NSCLC xenografts in vivoIndividual BALB/c nude mice were injected intravenously with 1×10 [6] XWLC-05-miR-370 or XWLC-05-miR-NC cells (n=4, per group). [score:5]
In this study, we found that miR-370 over -expression inhibited the proliferation, clonogenicity, wound healing and invasion of XWLC-05 and H157 cells in vitro. [score:5]
To induce miR-370 over -expression, XWLC-05 cells were transfected with pPG/miR-370/EGFP or control pPG/miR-NC/EGFP using Lipofectamin [TM] 2000 reagent for 24 h. The cells were treated with 6 ng/mL of blasticidin S (Sigma) for 30 days to establish stable XWLC-05-miR-370 over -expression and control XWLC-05-miR-NC cells. [score:5]
After being annealed, the DNA fragments were cloned at the SacI/XhoI sites of the pmiRGLO firefly luciferase -expressing vector (Promega, WI, USA) to generate plasmids of pmiRG-EGFR-UTR-wt, pmiRG-EGFR-UTR-mut and pmiRG-miR-370 -inhibitor-PC, respectively, followed by sequencing. [score:5]
MiR-370 over -expression inhibits the lung metastasis of xenograft NSCLC tumors in vivo. [score:4]
To test the function of miR-370 in lung cancer cells, XWLC-05 and H157 cells were transfected with miR-370 mimics, miR-370 inhibitor, control miR-NC or control inhibitor and the dynamic proliferation of different groups of cells was determined by MTT assay. [score:4]
Figure 4XWLC-05 and H157 cells were transfected with miR-370 mimics, miR-370 inhibitor or corresponding controls for 24 h. The relative levels of EGFR, HIF-1α, ERK, AKT expression, ERK and AKT phosphorylation were determined by assays. [score:4]
MiR-370 over -expression inhibits the lung metastasis of NSCLC xenografts in vivo. [score:4]
MiR-370 over -expression inhibits the growth and angiogenesis of xenograft NSCLC tumors in vivo. [score:4]
XWLC-05 and H157 cells were transfected with miR-370 mimics, miR-370 inhibitor or corresponding controls for 24 h. The relative levels of EGFR, HIF-1α, ERK, AKT expression, ERK and AKT phosphorylation were determined by assays. [score:4]
XWLC-05 and H157 cells (1×10 [5]/well) were cultured in 24-well plates overnight and co -transfected in triplicate with 250 ng pmiRG-EGFR-UTRwt, pmiRG-EGFR-UTRmu or pmiRG-miR-370 -inhibitor-PC, together with 20 nM miR-370 mimic or miR-NC, by Lipofectamine 2000 according to the manufacturer's instructions. [score:3]
XWLC-05 cells were transfected with pre-miR-370 or miR -negative control (miR-NC) to establish stable XWLC-05-miR-370 over -expression and control XWLC-05-miR-NC cells. [score:3]
In comparison with the controls transfected with miR-NC, transfection with miR-370 mimics significantly reduced the relative levels of EGFR and HIF-1α expression, reduced AKT and ERK1/2 phosphorylation in XWLC-05 and H157 cells (Figure 4). [score:3]
More importantly, transfection with miR-370 significantly reduced the EGFR 3′UTR-wt-regulated luciferase activity, but did not affect the EGFR 3′UTR-mut-regulated luciferase activity in both XWLC-05 and H157 cells. [score:3]
Modulation of miR-370 expression alters the neoplastic behaviors of lung cancer XWLC-05 and H157 cells in vitro. [score:3]
The cells were treated with 6 ng/mL blasticidin for 30 days to establish stable miR-370 over -expressing XWLC-05-miR-370 and control XWLC-05-miR-NC cells. [score:3]
Transfection with miR-370 mimics, inhibitors. [score:3]
In comparison with the controls transfected individual plasmids with miR-NC, transfection with miR-370 mimics, together with pmiRG-EGFR-UTRwt or pmiRG-miR-370 -inhibitor-PC, but not pmiRG-EGFR-UTRmu significantly reduced the levels of luciferase activity in both XWLC-05 and H157 cells (Figure 2C and 2F). [score:3]
Therefore, miR-370 may be a tumor suppressor and our findings may aid in design of new therapeutic strategies for intervention of lung cancers. [score:3]
XWLC-05 and H157 cells were transfected with miR-370 mimics, miR-370 inhibitor, or corresponding scrambled controls for 24 h. The different groups of cells (10 [4] cells/well) were cultured in 96-well plates for 4 days and the cell viability of each group of cells was determined in triplicate using 3-(4, 5-dimethyl-thiazol-2-yl) 2, 5-diphenyltetrazolium bromide (MTT) reagent (Sigma). [score:3]
Next, we examined the relative levels of EGFR to control β-actin expression and miR-370 to U6 transcripts in human lung cancer A549, H460, H157, XWLC-05 cells, and non-tumor bronchial epithelial Beas-2b cells by and quantitative RT-PCR, respectively. [score:3]
In this study, we found that the 3′UTR of the EGFR contained a potential binding site of miR-370 and the levels of EGFR were negatively associated with the levels of miR-370 expression in several human lung cancer cell lines and non-tumor bronchial epithelial cells. [score:3]
We synthesized the EGFR 3′UTR mutant at the potential binding sequence of miR-370 (Figure 2G) and generated pmiRG-EGFR-UTRwt, pmiRG-EGFR-UTRmu and pmiRG-miR-370 -inhibitor-PC plasmids. [score:3]
XWLC-05 and H157 cells were cultured in medium without antibiotics overnight and transfected with 20 nM miR-370 mimics, 40 nM miR-370 -inhibitor, or their corresponding scrambled controls for 24 hours using the Lipofectamine TM 2000 transfection reagent (Invitrogen). [score:3]
EGFR and miR370 expression in lung cancer cells. [score:3]
We found that XWLC-05-miR-370 cells displayed higher levels of miR-370, but lower EGFR expression than control XWLC-05-miR-NC cells (Figure 5A, 5B and 5C). [score:3]
In summary, our data suggest a negative association between the levels of EGFR and miR-370 expression in human lung cancer cell lines and non-tumor bronchial epithelial cells. [score:3]
Modulation of miR-370 alters the EGFR expression in lung cancer cells. [score:3]
The EGFR and miR-370 expression in different lung cancer cells and non-tumor bronchial epithelial cells. [score:3]
These consistent with previous findings and support the notion that miR-370 is a tumor suppressor of cancer [36– 38]. [score:3]
Subsequently, we transfected XWLC-05 and H157 cells with pmiRG-EGFR-UTRwt, pmiRG-EGFR-UTRmu or pmiRG-miR-370 -inhibitor-PC, together with miR-370 mimic or miR-NC for 48 h, respectively. [score:3]
In this study, we examined the levels of miR370 and EGFR expression in several human lung cancer cell lines and non-tumor bronchial epithelial cells, and explored the effect of miR-370 on the proliferation, angiogenesis and migration of lung cancer cells in vitro and the growth and metastasis of lung cancers in vivo. [score:3]
Immunohistochemistric analysis revealed that the percentages of EGFR+ or KI67+ cells and the levels of HIF-1α expression and microvessel density (MVD) in the XWLC-05-miR-370 tumor sections were significantly lower than that in the XWLC-05-miR-NC tumor sections (Figure 5H). [score:3]
MiR-370 over -expression inhibits the growth and angiogenesis of xenograft NSCLC tumors in vivoNext, we evaluated the effects of miR-370 on the growth of NSCLC xenografts in vivo. [score:3]
Hence, the levels of miR-370 expression may be negatively associated with the levels of EGFR in these cells, except for A549 cells. [score:3]
In addition, XWLC-05 and H157 cells were co -transfected in triplicate with pmiRG-EGFR-UTRwt, pmiRG-EGFR-UTRmut or pmiRG-miR-370 -inhibitor-PC, together with 20 nM miR-370 mimics or miR-NC for 48 h and the luciferase activities of individual cell samples were analyzed. [score:3]
Finally, we examined the effect of miR-370 over -expression on the lung metastasis of xenograft NSCLC tumors in vivo. [score:3]
These suggest that miR-370 may bind to the 3′UTR of EGFR mRNA and the miR-370 inhibitor in both lung cancer cells. [score:3]
XWLC-05 and H157 cells were transfected with miR-370 mimics, miR-370 inhibitor or their corresponding controls for 24 h. The proliferation, colony formation, wound healing and invasion of individual groups of cells were determined by MTT, colony formation, wound healing and transwell invasion assays, respectively. [score:2]
Figure 3XWLC-05 and H157 cells were transfected with miR-370 mimics, miR-370 inhibitor or their corresponding controls for 24 h. The proliferation, colony formation, wound healing and invasion of individual groups of cells were determined by MTT, colony formation, wound healing and transwell invasion assays, respectively. [score:2]
For luciferase reporter assay, oligonucleotides for the EGFR 3′-UTR wild type (WT), EGFR 3′-UTR mutant and Hsa-miR-370-3P inhibitor (as a positive control) were synthesized by Genepharma (Shanghai, China). [score:2]
The relative levels of miR-370 transcripts and EGFR expression in XWLC-05-miR-370 and control XWLC-05-miR-NC cells were determined by quantitative RT-PCR and assays, respectively. [score:2]
MiR-370 over -expression attenuated the growth, angiogenesis and metastasis of implanted lung tumors in vivo. [score:2]
BALB/c nude mice were injected intravenously with XWLC-05-miR-370 or XWLC-05-miR-NC cells. [score:1]
We found that the volumes of XWLC-05-miR-370 tumors were significantly smaller than XWLC-05-miR-NC tumors at day 11, 14, 17 and 20 post implantation (Figure 5D and 5E). [score:1]
The body weights of the mice bearing XWLC-05-miR-370 tumors were significantly higher than that of those bearing XWLC-05-miR-NC tumors (Figure 6A). [score:1]
Individual female BALB/c nude mice were implanted subcutaneously with 2×10 [6] XWLC-05-miR-370 or XWLC-05-miR-NC cells (n=4, per group). [score:1]
We found that the 3′UTR of the EGFR contained the potential binding site of miR-370 using several online database (http://www. [score:1]
Next, female BALB/c nude mice were implanted subcutaneously with 2×10 [6] XWLC-05-miR-370 or XWLC-05-miR-NC cells/mouse (4 mice per group). [score:1]
At the end of the experiment, the XWLC-05-miR-370 tumor weights were significantly less than XWLC-05-miR-NC tumors (Figure 5F). [score:1]
To establish stable transfected cells, pre-miR-370 or miR -negative control (miR-NC) were cloned into the plasmid pPG/miR/EGFP (Genepharma). [score:1]
These independent lines of data indicated that miR-370 attenuated the EGFR-related ERK1/2 and AKT signaling in lung cancer cells in vitro. [score:1]
Individual BALB/c nude mice were injected intravenously with 1×10 [6] XWLC-05-miR-370 or XWLC-05-miR-NC cells (n=4, per group). [score:1]
Next, we tested whether miR-370 affected the EGFR 3′UTR-regulated luciferase activity by dual-luciferase reporter assay. [score:1]
There were obviously more tumor nodules in the lungs of the mice bearing XWLC-05-miR-NC tumors than those bearing XWLC-05-miR-370 tumors. [score:1]
Therefore, currently, the role of miR-370 in the tumorigenesis and metastasis of lung cancers remains controversial. [score:1]
The impact of miR-370 on the metastasis of implanted tumors was determined. [score:1]
To establish a subcutaneous tumor mo del in nude mice, XWLC-05 cells were transfected with pre-miR-370 or miR -negative control (miR-NC). [score:1]
Individual mice were implanted subcutaneously with 2×10 [6] XWLC-05-miR-370 or XWLC-05-miR-NC cells (4 mice per group). [score:1]
Briefly, individual mice were injected intravenously with 1×10 [6] XWLC-05-miR-370 or XWLC-05-miR-NC cells (4 mice per group). [score:1]
Analysis of the tumor tissues indicated that the relative levels of EGFR mRNA transcripts in the XWLC-05-miR-370 tumors were significantly lower than XWLC-05-miR-NC tumors (Figure 5G). [score:1]
In contrast, high levels of miR-370 transcripts were detected in H460, Beas-2b, A549 and moderate levels of miR-370 in H157 cells while much lower levels of miR-370 in XWLC-05 cells (Figure 1D). [score:1]
A previous study has showed that miR-370 may have a causative role in the disorder of lipid metabolism [22]. [score:1]
The micrometastases were scored according to the reference [32], and quantitative analysis revealed that the scores of lung metastatic tumors in the mice bearing XWLC-05-miR-370 tumors were significantly less than those bearing XWLC-05-miR-NC tumors (Figure 6C). [score:1]
Figure 1 (A) A potential binding site of miR-370 in the 3′UTR of the EGFR was predicted using online tools. [score:1]
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[+] score: 183
Other miRNAs from this paper: hsa-mir-214, mmu-mir-214, hsa-mir-370
We assessed the level of expression of miR-370 and SLD5 by qRT-PCR using tumor tissue on day 20 after treatment, and confirmed overexpression of miR-370 and downregulation of SLD5 in tumors from the miR-370 -injected group. [score:8]
A miRNA-370 mimic inhibits tumor growth in vivo In vitro experiments had clearly demonstrated that overexpression of miR-370 suppresses proliferation of cancer cells. [score:7]
The results suggested that miR-370 inhibits mRNA expression in T24 cells, resulting in a reduction of SLD5 protein expression. [score:7]
After 24 hours of treatment with 5-aza, miR-370 expression was more strongly induced in cancer cells than in control cells (Fig. 6A), suggesting that its expression is suppressed in cancer cells by DNA methylation. [score:7]
We found that attenuated miR-370 expression in cancer cells is partly mediated by methylation of the miR-370 promoter, because treatment with 5-aza-2-deoxycytidine (5-aza), a specific inhibitor of DNA methylation 34, induced the expression of this miRNA. [score:7]
Consistent with this, knocking down IL-6 using siRNA resulted in reduced DNMT1 expression (Fig. 6E,F) and concurrent upregulation of miR-370 (Fig. 6G) and reduction of SLD5 (Fig. 6H). [score:7]
miR-370 downregulation results in SLD5 upregulation in human bladder cancer cells. [score:7]
In contrast, in bladder cancer cells, miR-370 is downregulated, and SLD5 expression levels are increased to induce proliferation of cancer cells. [score:6]
We analyzed whether miR-370 expression is regulated by DNA methylation by using 5-azacytidine (5-aza), an inhibitor of DNA methylation. [score:6]
These results suggest that hypermethylation caused by IL-6 induces suppression of many genes including miR-370, contributing to the upregulation of SLD5. [score:6]
As observed in the siRNA experiments (Fig. 2), miR-370 overexpression also inhibited the proliferation of bladder cancer cells (Fig. 4F). [score:5]
Because endothelial cells, blood cells (data not shown) and fibroblastic cells 33 express GINS complex gene, reduced SLD5 expression by the injection of miR-370 caused attenuation of cellular activity of those cells and cancer cell proliferation and survival could not be supported by such stromal cells. [score:5]
In vitro experiments had clearly demonstrated that overexpression of miR-370 suppresses proliferation of cancer cells. [score:5]
The results suggested that inhibition of miR-370 led to increased SLD5 mRNA and protein expression in normal cells. [score:5]
In normal cells, SLD5 expression is blocked by miR-370 expression. [score:5]
However, in cancer cells, IL-6 induces DNMT1 to inhibit miR-370 expression. [score:5]
Because miR-370 suppresses SLD5, in cancer cells SLD5 expression is restored and cells can proliferate. [score:5]
We confirmed that miR-370 expression was indeed suppressed in T24 and KMBC2 cells (Fig. 4A,B). [score:5]
Based on our results, we hypothesize that miR-370 acts as a negative regulator of SLD5 expression in normal states. [score:4]
We knocked down miR-370 in normal cell lines (HUVEC) using miR-370 inhibitor transfection methods and assessed SLD5 mRNA and SLD5 protein levels using qRT-PCR and, respectively (Supplementary Fig. 3). [score:4]
Furthermore, we identified miR-370 as a negative regulator of SLD5 gene expression. [score:4]
SLD5 mRNA expression is regulated by miR-370. [score:4]
It has also been suggested that miR-370 is normally imprinted and activated only on the maternal allele 35, so it may be predicted that miR-370 is downregulated even when CpG islands are only slightly methylated. [score:4]
Regulation of miR-370 expression in tumors. [score:4]
How to cite this article: Yamane, K. et al. Regulation of SLD5 gene expression by miR-370 during acute growth of cancer cells. [score:4]
Among several candidates, we found that a miR-370 target sequence is located at the 3′-UTR of the SLD5 gene. [score:3]
After injection of miR-370, tumor growth was clearly suppressed (Fig. 5A,B). [score:3]
A miRNA-370 mimic inhibits tumor growth in vivo. [score:3]
In Fig. 4, overexpression of miR-370 might affect not only cancer cells but other cells consisting cancer microenvironment. [score:3]
T24 cancer cells were transfected with pMIR luciferase vector with an inserted 3′-UTR region of SLD5 containing the miR-370 target sequence. [score:3]
Moreover, we confirmed that SLD5 protein was also suppressed in tumor tissue of miR-370 -injected relative to control tumors (Fig. 5C,D). [score:3]
Although we focused on miR-370, it is possible that there are multiple additional miRNAs that are relevant for SLD5 expression in vivo. [score:3]
In terms of the cell cycle, similar to the results from the SLD5 knockdown study, miR-370 mimic transfection reduced the fraction of cells in S phase relative to control miR transfection (Fig. 4I). [score:2]
Regulation of miR-370 in human bladder cancer cells. [score:2]
The 3′ UTR region of SLD5, containing miR-370 target sites, was amplified using a standard PCR protocol with the following linker primers: 5′-ATT ACT ACT AGT GCA TAA ACA GCC AGG CAT GGT GAC-3′ (forward), 5′-AAC CAT AAG CTT TAG TAG AGA TGG GTT TAG TAG AG-3′ (reverse). [score:2]
Therefore, we conclude that miR-370 directly binds to the 3′-UTR of the SLD5 gene. [score:2]
Addition of a miR-370 mimic led to reduction of the luciferase activity of the SLD5 3′-UTR, whereas miR-214 as a negative control had no affect (Fig. 4C). [score:1]
The present study revealed a relationship between SLD5 and miR-370 in human bladder cancer. [score:1]
After 24 h, miRNA was isolated and cDNA synthesized for qRT-PCR analysis of miR-370. [score:1]
Next, we investigated how miR-370 affects SLD5 expression. [score:1]
The Pre-hsa-miR-370 mimic (GeneDesign, Osaka, Japan) was transfected into T24 bladder cancer cells following the manufacturer’s instructions. [score:1]
Two weeks after transplantation, the developed tumors were treated with control scrambled RNA, SLD5 siRNA, or miR-370 mimic suspended in atelocollagen (Atelogene, KOKEN, Tokyo, Japan) to facilitate siRNA introduction into tumors, according to the manufacturer’s instructions Twenty days after atelocollagen injection, xenograft tumor volumes and weights were measured, RNA was isolated from tumors for the analysis of SLD5 or miR-370 expression by qRT-PCR, and tumor tissues were fixed in 4% paraformaldehyde for immunohistochemistry analysis. [score:1]
T24 bladder cancer cells were plated in 96-well plates and transfected with or without miR-370 mimic and luciferase vector. [score:1]
miR-370 mimics or control miR were injected on day10 post-inoculation. [score:1]
To assess this, T24 cells were inoculated into nude mice and control miR or miR-370 mixed with atelocollagen was injected into the tumors once they had reached approximately 50 mm [3] in diameter. [score:1]
Tumor growth is affected by miR-370. [score:1]
Moreover, we analyzed cell kinetics and how the cell cycle was affected by miR-370. [score:1]
To document direct binding of miR-370 to the 3′-UTR of the SLD5 gene, we performed luciferase reporter assays. [score:1]
Cells were analyzed after transfection with control or miR-370 mimic. [score:1]
Therefore, bladder cancer cells may have intrinsic signaling pathways for methylating the miR-370 promoter region. [score:1]
T24 cells were transfected with pMIR luciferase reporter containing 3′-UTR sequences of SLD5 and miR-370. [score:1]
Next, we investigated whether miR-370 can effectively inhibit tumor growth in vivo. [score:1]
Next, we investigated whether miR-370 silencing affects SLD5 expression in normal cells. [score:1]
The level of miR-370 (left) and SLD5 (right) after transfection of each miR was confirmed by qRT-PCR. [score:1]
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[+] score: 128
This dysregulates cell survival by targeting the newly discovered targets, SHMT-2 and MECP-2, respectively; apoptosis was induced by the inhibition of miR-370 or miR-373, and also by the overexpression of SHMT-2 or MECP-2. These results suggest that the decreased functions of miR-370 and miR-373 in OA chondrocytes lead to the disinhibition of SHMT-2 and MECP-2, respectively, thereby promoting apoptotic cell death. [score:12]
Co-induction of miR-370 significantly inhibited SHMT-2 -induced MMP-13 expression and SHMT-2 -upregulated apoptosis-related gene cell death in normal chondrocytes (Fig. 4D). [score:8]
The previously identified targets for miR-370 and miR-373 were largely associated with cancer pathogenesis (e. g., oncogenes and tumor suppressors), suggesting that the utilized target genes may contribute to the tissue- and cell-type-specific performances of these miRNAs (Akhtar et al., 2010). [score:7]
miRNA inhibitor -mediated knockdown and pre-miR-370/373 -mediated upregulation of miR-370 and miR-373. [score:7]
To further test whether MECP-2 is a target of miR-370 or miR-373, we cloned the entire 3′UTR of MECP-2 into a luciferase reporter vector, electroporated the vector into chondrocytes along with the precursor of miR-370 or miR-373 or a cognate nontargeting negative control, and assayed cell lysates for luciferase expression. [score:6]
Fig 4miR-370 regulates OA pathogenesis by targeting SHMT-2. (A) Luciferase reporter activity was driven by the 3′UTR of SHMT-2 or mutated 3′UTR of SHMT-2 (3′UTR mt) with or without forced expression of miR-370 (left panel). [score:6]
Normal and OA chondrocytes were treated with a miR-370 precursor (miR-370) or an inhibitor of miR-370 (anti-miR-370), and the protein expression levels of MMP-2 and MMP-13 were analyzed by immunoblotting. [score:5]
To see whether these two OA-specific miRNAs are involved in the regulation of SHMT-2, we cloned the entire 3′UTR of SHMT-2 into a luciferase reporter vector, electroporated the vector into cells along with the precursor of miR-370 or a cognate nontargeting negative control, and assayed cell lysates for luciferase expression. [score:5]
For example, miR-370 targets FOXO1 in gastric mucosal cancer and has been associated with disease progression (Voorhoeve et al., 2007). [score:5]
On the other hand, inhibition of miR-370 in OA chondrocytes increased the expression levels of these proteins. [score:5]
In sum, we herein show for the first time that miR-370 and miR-373 directly target and negatively regulate SHMT-2 and MECP-2, respectively, in human articular chondrocytes, where they contribute to the pathogenesis of OA. [score:5]
Overexpression of miR-370 suppressed the RNA levels of apoptosis-related and autophagy-related genes (Fig. 4C). [score:5]
Here, we present the first evidence suggesting that miR-370 and miR-373 may potently regulate one-carbon metabolism by directly targeting SHMT-2 and MECP-2, respectively. [score:5]
However, the induction of miR-370 in OA chondrocytes significantly reduced this apoptotic cell death to 4.56%, whereas inhibition of miR-370 increased cell death among OA chondrocytes. [score:3]
We identify serine hydroxymethyltransferase (SHMT)-2 and methyl-CpG -binding protein (MECP)-2 as targets of miR-370 and miR-373, respectively, and hypothesize that these interactions contribute to the pathogenesis of OA. [score:3]
The precursors or inhibitors of miR-370 and miR-373 (Ambion, Austin, TX, USA) were electroporated into cells using a square-wave generator (BTX-830; Gentronics, San Diego, CA, USA) with 20 ms, 200 square pulses. [score:3]
We found that chondrocytes transfected with the SHMT-2 3′UTR -driven vector plus pre-miR-370 exhibited significantly less luciferase activity but mutated SHMT-2 3′UTR -driven vector plus pre-miR-370 did not alter luciferase activity (Fig. 4A, left panel) compared to cells that received the reporter plus the nontargeting negative control, suggesting that miR-370 may be involved in the SHMT-2-regulated pathogenesis of OA. [score:3]
Furthermore, decreased levels of miR-370 and miR-373 were observed in OA chondrocytes from majority of patients, as confirmed by analysis of MMP-13 expression (Fig. 3B). [score:3]
In in vivo study using DMM mice, the most severe cartilage destruction (as visualized by safranin O staining) was observed among mice infected with anti-miR-370- and SHMT-2-encoding lentiviruses, whereas infection of DMM mice with miR-370 -expressing lentiviruses significantly ameliorated DMM -induced cartilage destruction (Fig. 4F). [score:3]
OA chondrocytes were treated with miR-370 precursor (miR-370) and miR-370 inhibitor (anti-miR-370), and SHMT-2 level was analyzed by real-time PCR (right panel). [score:3]
Finally, we propose that miR-370 and miR-373 could be potent therapeutic targets for OA. [score:3]
For miRNA target validation, cells were electroporated as described above with 25–50 ng of each firefly luciferase reporter construct, 150–175 ng of empty pcDNA3 vector (Clontech, Mountain View, CA, USA), 200 ng pcDNA3 harboring the Renilla luciferase gene (transfection control), and 30 pmol of pre-miR-370, pre-miR-373, or pre-miR-neg (Ambion). [score:3]
Here, we found that miR-370 and miR-373 were significantly downregulated in OA chondrocytes compared to normal chondrocytes. [score:3]
To investigate whether modulation of miR-370 induced the same effects as modulation of SHMT-2, we altered the expression level of miR-370 using its specific inhibitor or precursors (Fig. 4B). [score:3]
Annexin V staining revealed that the induction of miR-373 in OA chondrocytes significantly reduced this apoptotic cell death to 2.26%, whereas inhibition of miR-370 increased cell death up to 10% in normal chondrocytes. [score:3]
These results provide novel insights into OA and may facilitate the development of therapeutic approaches based on the modulation of miR-370 and/or miR-373. [score:2]
In addition, induction of miR-370 decreased SHMT-2 RNA level, whereas knockdown of miR-370 increased SHMT-2 RNA level in OA chondrocytes (Fig. 4A, right panel). [score:2]
Here, we report the first study showing that the levels of miR-370 and miR-373 are significantly lower in OA chondrocytes. [score:1]
of miR-370 as confirmed by real-time PCR into OA chondrocytes reduced the protein levels of MMP-2 and MMP-13 that are typically increased in OA chondrocytes. [score:1]
Among we analyzed, miR-370 and miR-373 seem highly OA specific (Fig. 3A). [score:1]
In this prospective study, we examined the potential functional role of miR-370 and miR-373 in OA pathogenesis. [score:1]
In addition, folate treatment reduced miR-370 levels and apoptosis of OA chondrocytes (Fig. 4E), suggesting that miR-370 may be involved in one-carbon metabolism. [score:1]
Human 293FT cells were transfected with lentiviral vectors encoding miR-370, miR-373, SHMT-2, or MECP-2 or the negative control lentivirus (Applied Biological Materials, Canada) using the third-generation packaging mix (Applied Biological Materials, Canada) and Lentifectin (Applied Biological Materials, Canada). [score:1]
DMM surgery was performed in male mice, and lentiviruses were injected intra-articularly with 1 × 10 [9] plaque-forming units (PFU) of lentiviral vectors encoding miR-370, miR-373, SHMT-2, or MECP-2 every week for 8 weeks. [score:1]
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4
[+] score: 91
Other miRNAs from this paper: mmu-mir-122
Surprisingly, miR-122 and miR-370 levels seem to be also modulated by maternal milk, since pups from control dams suckled by HFD-fed dams showed a decrease in miR-122 and increased expression of hepatic miR-370 as well as upregulation of TAG synthesis markers (Agpat and Gpam) and downregulation of a fatty oxidation marker (Acadvl). [score:9]
Offspring from HFD-fed dams present downregulation of hepatic β-oxidation-related genes and upregulation of genes involved in lipid synthesis, and these alterations seem to be driven by the modulation of miR-122 and miR-370 levels, causing metabolic adaptations that lead to increased ectopic lipid accumulation in the liver of recently weaned mice [25]. [score:7]
Additionally, Xu and colleagues showed that inhibition of miR-370 led to downregulation of pro-inflammatory cytokines, suggesting that this miRNA plays a pro-inflammatory role and may be related to hepatic damage [57]. [score:6]
miR-122 is predicted to modulate lipogenic genes and to be potentially targeted by miR-370 which, in turn, can directly bind to carnitine palmitoyltransferase 1α (Cpt1a) gene [20, 21]. [score:4]
Furthemore, maternal FFA at gestation correlated directly with miR-370 and inversely with miR-122 in the liver of newborns, thus reinforcing the hypothesis that maternal lipids that cross placental barrier are able to modulate miRNAs expression of offspring. [score:4]
Besides, offspring from HFD-dam presents altered serum lipid levels [25] and here, offspring's serum TAG correlated directly with miR-370 and inversely with miR-122 hepatic expression. [score:4]
Interestingly, hepatic miR-122 expression was significantly reduced in CH (2.2-fold), HH (1.5-fold) and HC (2.1-fold) compared to CC, while mir-370 expression was significantly increased in CH (4.4-fold), HH (7.7-fold) and HC (8.9-fold) (Fig.   4i), corroborating the data showing that HFD feeding at gestational period leads to alterations in these miRNAs in offspring and also showing that excessive lipids consumption at lactation period can also lead to these miRNAs modulation. [score:4]
Interestingly, adult offspring from HFD-fed dam still shows decreased miR-122 and increased miR-370 expression in the liver. [score:3]
Maternal HFD consumption in gestational or suckling periods independently alters miR-122 and miR-370 and lipid-related gene expression in the liver of recently weaned offspring. [score:3]
using liver cell line showed that palmitate could induced decrease in miR-122 and increase in miR-370 expression. [score:3]
The treatment lead to a decreasing in miR-122 (among 13 to 39%) and an increasing in miR-370 levels (among 31 to 114%; Fig.   2a and b, respectively), indicating that excessive fat could alter the expression of these miRNAs in liver. [score:3]
The presence of fatty acids in maternal blood and milk seem to be responsible for modulating the expression of miR-122 and miR-370, which are involved in liver metabolism. [score:3]
In a recent study, we showed that maternal HFD consumption during pregnancy and lactation leads to a decreased miR-122 and increased miR-370 expression in the liver of recently weaned mice [25]. [score:3]
Different letters indicate statistical significance between groups (p ≤ 0.05) Importantly, the modulation of hepatic miRNAs by maternal HFD consumption at gestation and lactation also persists to adult life, since HH showed lower miR-122 (42%) and higher miR-370 (139%) expression in comparison to CC at d82 (Fig.   5i). [score:3]
Although the relationship between the levels of miR-122 and miR-370 is still subject to debate [14, 19], we showed that there is an inverse expression of these miRNA in our mo del at different ages. [score:3]
Different letters indicate statistical significance between groups (p ≤ 0.05) Importantly, the modulation of hepatic miRNAs by maternal HFD consumption at gestation and lactation also persists to adult life, since HH showed lower miR-122 (42%) and higher miR-370 (139%) expression in comparison to CC at d82 (Fig.   5i). [score:3]
The presence of fatty acids in maternal blood and milk seem to be responsible for modulating the expression of liver miR-122 and miR-370, which are involved in liver homeostasis. [score:3]
Moreover, maternal consumption of a HFD during gestation provoked a decrease in miR-122 (50%) and an increase in miR-370 (206%) expression (Fig.   3h). [score:3]
To test the hypothesis that fatty acids could modulate the expression of hepatic miR-122 and miR-370, we performed in vitro analysis in mouse (Hepa1c1c7) and human (HepG2) hepatoma cell lines treated with palmitate. [score:3]
miR-122 and miR-370 participate in the regulation of hepatic lipid metabolism [20– 26]. [score:2]
The relative expression of miR-122 and miR-370 (ID 002245 and ID 002275, respectively, Thermo Fisher Scientific) was determined using primers with a TaqMan detection system and U6 spliceosomal RNA (ID 001973, Thermo Fisher Scientific) as endogenous controls. [score:2]
Thus, the aim of the present study was to test the hypothesis that maternal high fat diet could directly modulate miR-122 and miR-370 expression and to investigate the independent contribution of pregnancy and lactation to the altered hepatic lipid metabolism observed in young offspring from obese dams. [score:2]
In vitro hepatocytes treatment with palmitate alters miR-122 and miR-370 levels. [score:1]
As we have speculated, miR-122 and miR-370 may be involved in the impairments of lipid homeostasis of newborns from HFD-fed dams, since we find here that these miRNAs are modulated at d0, as early as the hepatic enzymes involved in lipid metabolism. [score:1]
Body weight (a), adiposity (b), caloric intake (c), fasting glucose (d) and serum lipids (CHOL and TAG - e), mRNA levels (qRT-PCR) of hepatic Cpt1a and Acadvl (f), and Agpat and Gpam (g), hepatic total lipid content (h), microRNA level (qRT-PCR) of hepatic miR-122 and miR-370 (i), correlation analysis between hepatic miR-122 and serum TAG (j) from recently weaned unfostered offspring (CC and HH) and crossfostered offspring (CH and HC) at d28. [score:1]
Body weight (a), adiposity (b), caloric intake (c), fasting glucose (d), mRNA levels (qRT-PCR) of hepatic Cpt1a and Acadvl (e) and Agpat and Gpam (f), serum lipids (CHOL and TAG - g), total hepatic lipid content (h), microRNA level (qRT-PCR) of hepatic miR-122 and miR-370 (i) from adult offspring from CC and HH groups at d82. [score:1]
Newborn pups (d0) from obese dams showed a decrease in lipid oxidation markers (Cpt1a and Acadvl), an increase in triacylglycerol synthesis markers (Agpat and Gpam), as well as lower miR-122 and higher miR-370 hepatic content that was inversely correlated to maternal serum NEFA and TAG. [score:1]
MicroRNA level (qRT-PCR) - miR-122 and miR-370 - from Hepa1c1c7 mouse hepatoma cell line (1x10 [8]cells/mL) (a) and HepG2 human hepatoma cell line (1x10 [8]cells/mL) (b) 6hs after exposure to palmitic acid (500uM). [score:1]
Therefore we hypothesized that the lipids consumed by the dams, specially SFA, could be responsible for miR-122 and miR-370 modulation in the liver of offspring through placental delivery during gestation and/or milk composition during suckling period. [score:1]
Here we evaluated whether maternal HFD consumption during gestation and lactation could differently affect liver miR-122 and miR-370 expression leading to metabolic damages observed in offspring. [score:1]
As shown in the present study, treatment with palmitic acid, one of the most abundant SFAs in the human diet and blood, leads to a decrease in miR-122 and increased miR-370 levels in hepatocytes. [score:1]
Body weight (a), lee index of obesity (LIO) (b), serum lipids (CHOL and TAG - c), fasting glucose (d) and serum insulin (e), mRNA levels (qRT-PCR) of hepatic Cpt1a and Acadvl (f), and Agpat and Gpam (g), microRNA level (qRT-PCR) of hepatic miR-122 and miR-370 (h) from newborn offspring from C and H groups. [score:1]
However, although our previous results reports that miR-122 and miR-370 may participate in the genesis of metabolic damage associated to fatty liver [25], it is not possible to assign the role of gestational or lactational periods to the effects observed in offspring from obese dams and literature data concerning these phenomena are very controversial. [score:1]
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5
[+] score: 43
Along the same lines, DRGs from mice injected intrathecally with miRNA mimics showed a strong expression of targeted miRNAs in comparison to corresponding non -targeting mimics (examples with overexpression of miR-370-3p and miRNA-291b-5p with their respective mimics in comparison with non -targeting-controls is shown in Fig 2, panel D; p < 0.05 two tailed t-test). [score:11]
This was also evident upon comparing response thresholds (Fig 4, panel B) or AUC (Supporting Information Fig 3, panel A) of stimulus–response frequency curves over von Frey forces 0.02–1 g. Thus, counteracting tumour -induced downregulation of miR-370-3p and overexpressing it in DRGs led to exaggerated tumour -associated pain, indicating that downregulation of miR-370-3p constitutes an endogenous defense mechanism against tumour-pain. [score:9]
Interestingly, mice treated with a miR-370-3p -mimic developed significantly more tumour -induced mechanical hypersensitivity to a von Frey force of 0.02 g than mice treated with a non -targeting control mimic (Fig 4, panel A; p < 0.05). [score:3]
Further detailed analyses will reveal which of these putative targets mediate the pronociceptive functions of miR-34c-5p and miR-370-3p in the context of cancer pain. [score:3]
In contrast, augmenting the expression of miR-370-3p in DRGs led to exaggerated tumour -mediated hyperalgesia. [score:3]
In panel (C), * denotes p = 0.02 for miR-1a-3p, 0.04 for miR-34c-3p as compared to corresponding mismatch inhibitor and in panel (D), * denotes p = 0.001 for miR-370-3p and <0.0001 for miR-291b-5p as compared to non -targeting mimic, ANOVA followed by post hoc Fischer's test, n = 3 per group. [score:3]
Similarly, miR-370-3p, which was known in the context of angina pectoris and tumour suppression so far (Hoekstra et al, 2010; Zhang et al, 2012), emerged as a pro-nociceptive miRNA. [score:3]
Figure 4Change in frequency of paw withdrawal to plantar application of a von Frey filament force of 0.02 g following induction of tumor growth in the calcaneous bone of the heel in mice receiving intrathecally delivered miR-370-3p mimic (red symbols) or non -targeting mimic (green) or vehicle (grey symbols). [score:3]
Change in frequency of paw withdrawal to plantar application of a von Frey filament force of 0.02 g following induction of tumor growth in the calcaneous bone of the heel in mice receiving intrathecally delivered miR-370-3p mimic (red symbols) or non -targeting mimic (green) or vehicle (grey symbols). [score:3]
Following our protocol, we identified three miRNAs namely miR-1a-3p, miR-34c-5p and miR-370-3p to be enhancing tumour-pain and miR-483-3p to counteract it. [score:1]
miRIDIAN microRNA mimics for mmu-miR-370-3p (C-310619-07), miR-483* (C-310641-07) and miR-291b-5p (C-310666-03) were further custom -modified with 3′-cholesterol conjugation on passenger strand and 3′-FITC conjugation on guide strand to facilitate the in vivo uptake and facilitate visualization, respectively. [score:1]
[1 to 20 of 11 sentences]
6
[+] score: 38
According to previous studies, miR-370 is a lipid metabolism-related miRNA [56] and the increased miR-370 expression in hyperlipidemia patients has been positively correlated with the severity of coronary artery disease [57]. [score:5]
However, only miR-370 and miR-134 show enhanced expression levels in dmECFCs. [score:3]
Overexpression of miR-134, but not of miR-370, in dfECFCs results in decreased cell migration and poorer tube formation ability (Fig 3A). [score:3]
After overexpression of these two miRNAs in dfECFCs, miR-370 and miR-134 were 11-fold and 3.6-fold increased respectively (S4A Fig). [score:3]
MicroRNA-370 controls the expression of microRNA-122 and Cpt1alpha and affects lipid metabolism. [score:3]
Cell motility and microvasculature formation were then determined and it was found that miR-134 reduced cell migration by 34% and tube formation ability by 51%, while overexpression of miR-370 in dfECFCs resulted in no significant change (Fig 3A). [score:3]
Several genes, including sterol-regulatory element binding protein 1c (SREBP-1c), enzymes diacylglycerol acyltransferase-2 (DGAT2), fatty acid synthase (FAS) and acyl-CoA carboxylase 1 (ACC1), that are all involved in regulation of fatty acid and triglyceride biosynthesis, are increased by miR-370 in HepG2 cells. [score:3]
The effect of miR-370 and miR-134 overexpression on dfECFCs or HUVECs. [score:3]
miR-370 also targets carnitine palmitoyltransferase 1α (Cpt1α), which is a mitochondria enzyme and is involved in transportation of long-chain fatty acid for energy production, resulting in a decreased rate of beta oxidation [58]. [score:3]
Although dmECFCs show higher level of miR-370 than dfECFCs, it seems that miR-370 may also regulate other cellular mechanisms in DM. [score:2]
We validated these miRNA expression levels using four DF subjects’ ECFCs incubated under NG and HG condition and found that miR-370, miR-183-5p and miR-134 were increased under the HG condition compared to the NG treatment condition (Fig 2C), whereas the other seven miRNAs showed no statistically significant change (S3 Fig). [score:2]
S4 Fig (A) dfECFCs were infected with lenti-miR-370 and lenti-miR-134. [score:1]
We also measured the effect of miR-370 and miR-134 overexpression on cell motility and microvasculature formation of HUVECs (S4D Fig). [score:1]
0147067.g003 Fig 3. (A) Representative images (left) and quantitative data (right) from the Transwell migration assays (upper) and tube formation assays (lower) of dfECFCs with miR-370 and miR-134 overexpression. [score:1]
We have also identified that HG increases three miRNAs in ECFCs, namely miR-370, miR-183-5p and miR-134. [score:1]
Both miR-370 and miR-134 had no effect on cell proliferation or on cell cycle arrest (S4B and S4C Fig). [score:1]
[1 to 20 of 16 sentences]
7
[+] score: 35
Only 15 miRNAs from the 64 DEMs had validated target genes in IPA by target filter analysis, including miR-6349, miR-101a-3p, miR-6394, miR-126a-3p, miR-721, miR-143-3p, miR-497a-5p, miR-93-5p, miR-215-5p, miR-199a-3p, miR-23a-3p, miR-27b-3p, miR-2861, miR-30a-5p, and miR-370-3p. [score:5]
Among them, miR-370-3p was the most down-regulated serum exosomal miRNA by FMT treatment. [score:4]
Cyclin E and p21 were the predicted target genes of miR-370-5p in IPA dataset. [score:3]
Li L A Role of microRNA-370 in Hepatic Ischaemia-Reperfusion Injury by Targeting Transforming Growth Factor-Beta Receptor IILiver Int. [score:3]
Moreover, the reduced miR-370-3p in circulating exosomes may be the momentous event in aggravating cytotoxic effect of FMT by targeting p21 and Cyclin E. Figure 7 Ingenuity network diagram depicting interactions between the components of the p53 and Nrf2 -mediated oxidative stress signaling pathways. [score:3]
The liver injury is further intensified by the increased p21 and Cyclin E. A recent study also showed that restoration of reduced miR-370-3p had beneficial effects on the treatment of liver diseases [60], which was consistent with our results. [score:3]
Gong W Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells’ Malignancy by Activating miR-370/CCNE2 AxisFront Cell Neurosci. [score:2]
Lu CH MicroRNA-370 Attenuates Hepatic Fibrogenesis by Targeting SmoothenedDig Dis Sci. [score:2]
Xu WP Perturbation of MicroRNA-370/Lin-28 Homolog A/nuclear Factor Kappa B Regulatory Circuit Contributes to the Development of Hepatocellular CarcinomaHepatology. [score:2]
Both of these two pathways could be regulated by 8 miRNAs, and miR-370-3p was the most dramatically changed miRNAs (Table  5). [score:2]
Taken together, we present a schematic view of the pathways inside cells and pinpoint where miR-370-3p could perform its actions in Fig.   7. FMT -induced ROS generation causes DNA damage, which leads apoptosis through p53 -dependent mitochondrial damage and S-phase arrest. [score:1]
Interestingly, we notice that miR-370-3p in liver tissue did not show significant differences between the FMT -treated and control groups in our previous study [10]. [score:1]
miR-370-3p is a liver-abundant miRNA [60] that plays a pivotal role in the maintenance of liver homeostasis 61, 62. [score:1]
Actually, the interactions between miR-370-5p and these two target genes have been already verified by ChIP assay or luciferase reporter assay in previous study 63, 64. [score:1]
In this study, the administration of FMT decreases the level of circulating exosomal miR-370-5p. [score:1]
Although some specific cells probably internalize the circulating exosomes with lower miR-370-3p, the alterations of miR-370-3p are neutralized to changelessness when the whole liver is used as sample source. [score:1]
[1 to 20 of 16 sentences]
8
[+] score: 29
Other miRNAs from this paper: mmu-mir-122, mmu-mir-34a, mmu-mir-33
We examined both mRNA and protein levels of t-ACC and did not find any differences between the two groups; (2) significantly decreased expressions of miR-122 (61% decrease), miR-370 (64% decrease) and miR-33 (70% decrease), which involved in the regulation of lipid metabolism (Fig. 3B); 3) down-regulated the mRNA expression of genes related to fatty acid oxidation, such as carnitine palmytotransferase 1 (Cpt1α), peroxisome proliferator-activated receptor alpha (Pparα) and peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (Pgc1α) (Fig. 4A); (4) resulted in higher mRNA expression of liver X receptor α (Lxrα) and fatty acid translocase (Fat/ Cd36) (Fig. 4A); and 5) decreased mRNA expression of cholesterol efflux genes ATP -binding cassette sub -family G member 5 (Abcg5) and ATP -binding cassette sub -family G member 8 (Abcg8), and bile acid synthesis genes ATP -binding cassette sub -family G member 11 (Abcg11), cytochrome P450 (CYP)7A1 (Cyp7a1) and Cyp8b1 (Fig. 4B). [score:13]
The effects of miR-370 on fatty acids and hepatic TG accumulation might be through the modulation of miR-122 expression, as miR-370 up-regulates the expression of miR-122 49. [score:8]
Our present data showed the significantly decreased expression of miR-122, miR-370 and miR-33, accompanied with the increased expression of lipogenetic proteins ACC and SCD1 induced by HCLD feeding, supported the role of those miRNAs in the pathogenesis of hepatic steatosis. [score:5]
In the present study, we found the significantly decreased expression of miR-122, miR-370 and miR-33 after HCLD treatment, which may provide an additional mechanism regarding the hepatic steatosis induced by HCLD. [score:3]
[1 to 20 of 4 sentences]
9
[+] score: 23
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
qRT-PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats (Fig. 3 ). [score:7]
Real-time quantitative PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats. [score:7]
The levels of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377, and miRNA-96 were up-regulated, whereas miR-125b, miRNA-200b, miR-122, miRNA-466b, miR-138, miRNA-214, miRNA-503 and miRNA27a were down-regulated in response to 17α-E2 treatment. [score:7]
0078040.g003 Figure 3Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
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10
[+] score: 13
For example, restoration of miR-370 expression led to downregulation of FOXM1 in acute myeloid leukemia, promoting cell growth arrest and senescence [35]. [score:6]
The analysis of randomly-chosen miRNAs from clusters 1 and 2 (miR-654-3p, mir-369-3p, miR-495, miR-370-5p, miR-127-5p and miR-376c-3p) in tumor cell lines confirmed their downregulation (Figure 1d). [score:4]
Cahill and colleagues have shown that human derived BRAFT1799A- and RET/PTC-bearing thyroid tumor cells, KAT10 and TPC-1 respectively, express lower levels of 14q32-encoded miRNAs miR-323-3p, miR-370-5p, miR-127-3p, miR-299 and miR-154 [22, 23]. [score:3]
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[+] score: 10
Transfection of miR-323-5p (data not shown), miR-338-5p, and miR-370 plasmids did not affect the expression of luciferase reporter from constructs containing the respective target sequence in the 5′UTR (Fig S1A–B). [score:5]
miR-196b, miR-338-5p, miR-370 and miR-375 were previously reported to be expressed in adult mouse pancreas [22]. [score:3]
Four miRNAs (miR-196b, miR-323-5p, miR-338-5p and miR-370) with high complementarity to seed sequences (at least 5 base pairs between nucleotide position 2–8 of the miRNA) and a free energy of less than −22 kCal/Mole were selected (Table 1) for further analysis. [score:1]
Additionally, transfection of miR-370 and miR-338-5p duplexes did not show any significant change in reporter activity when transfected with insulin1 and insulin2-S reporters, respectively (Fig. S1C,D). [score:1]
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[+] score: 7
[43] miR-223 and miR-370 can directly target FOXO1 and regulate endogenous FOXO1 protein expression and are also responsible for cancer cell proliferation. [score:7]
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hsa-let-7c, hsa-miR-370, and hsa-miR-423-5p were strongly expressed in OFSCs (transcripts per million > 2,000) but each of them targeted only one gene, making them less possible as the key regulator in this study. [score:6]
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Within the miR-127 cluster, no miRNA targets were identified by miRNA/mRNA pairing (Figure 4C), while all had direct mRNA targets when miRNA/protein pairs were analyzed, such as miR-380-5p, miR-370, and miR-434. [score:6]
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Since possible target genes have been identified for only a few imprinted microRNAs, e. g. miR-134, miR-376a, miR-370, and the microRNAs embedded in the antisense transcript of the Retrotransposon-like 1 (Rtl1) gene [19, 22, 29- 32], we established a pipeline that combines different algorithms to predict microRNA target genes computationally. [score:5]
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This finding is particularly important given that a common Adeno-Associated Virus (AAV) insertion site in mice has recently been identified that maps between miR-341 and miR-370 in Meg8 that causes hepatocellular carcinomas, suggesting that perturbed expression of microRNAs may be responsible. [score:3]
Of note, miR-370 is also conserved in humans. [score:1]
Moreover, only Meg8 transcripts have the intron-encoded microRNAs miR-341, miR-1188, and miR-370 that lie upstream of Irm (see Figure 2 and Table 2). [score:1]
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[+] score: 5
Other miRNAs from this paper: hsa-mir-370, hsa-mir-373, hsa-mir-1180, hsa-mir-1236
And we also proved that miR-1236, miR-1180 and miR-370 could activate the expression of suppressor gene p21 [34– 36]. [score:5]
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Some miRNAs have been identified to regulate the expression of FoxM1, including miR-149, miR-134, miR-370, miR-494, miR-194, and miR-24-1 [37– 43]. [score:4]
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The bar graph of mir-370 expression in Figure 2H is an example of the pre-miRNA transcription pattern of this group. [score:3]
This group compromises 11 cellular pre-miRNAs: mir-7-2, mir-9-2, mir-30b, mir-107, mir-135a-2, mir-153-1, mir-153-2, mir-181b-2, mir-197, mir-325 and mir-370. [score:1]
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Three other miRNAs within this region (mmu-miR-673 and mmu-miR-370 flanking the core anti-Rtl1 cluster, and mmu-miR-409 at the distal end of the Mirg cluster) did not exhibit statistically significant differences in expression, suggesting that there may be tissue-specific cleavage of mature miRNAs from this region. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-370, ssc-mir-370
When cells reach to 80% confluence, 4 μg each of pCDH- METTL3-copGFP-Puro and pCDH-miR370-copGFP-Puro vectors were transfected into HEK-293T cells together with 4 μg pCL-Eco and 2 μg pCMV-VSV-G at a ratio of 2:2:1 using Lipofectamine 2000 (Invitrogen). [score:1]
To screening the stable pluripotent stem cell lines, lentiviral vectors pCDH- METTL3-copGFP-Puro and pCDH-miR370-copGFP-Puro were constructed for packing virus. [score:1]
The puromycin-resistant cell lines include J1 mES cells with miR370 transfection (J1/miR370), and porcine iPS cells with METTL3 transfection (piPS/METTL3) and with miR370 (piPS/miRNA370) (Fig.   5B). [score:1]
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Within the high homology regions, we found perfectly conserved seed matches for miRNAs that have been predicted (miR-103, miR-142-3p, miR-370, and miR-432) or already demonstrated (miR-15 [31], miR-16 [31], miR-26a [32], miR-214 [33], miR-548c-3p [34] and miR-761 [33]) to target the HMGA1 gene (Figure 1B and 1C). [score:3]
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Notably, microRNAs hsa-miR-127-5p, hsa-miR-370 and hsa-miR-376 had been shown to be highly and specifically expressed in islets of developing and adult human pancreas [53, 54]. [score:3]
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Among these miRNAs, four miRNAs, including miR-23a, miR-326, miR-346_MM 1 and miR-370, were further significantly downregulated by ischemic preconditioning compared with the levels in non-preconditioned controls. [score:3]
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In addition to miR-33a/b, miR-122, miR-370, miR-335, miR-378/378*, miR-27 and miR-125a-5p have been implicated in regulating cholesterol homeostasis, fatty acid metabolism and lipogenesis [9]. [score:2]
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Knockdown of long Non-Coding RNA KCNQ1OT1 restrained glioma cells' malignancy by activating miR-370/CCNE2 axis. [score:2]
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To search for a homologous human gene to mouse Rian, a 57-kb genomic region (−14 kb to +43 kb) around miR-370 of mouse (110,856,468–110,856, and 546 on NCBI M37/mm9) and corresponding human regions (101,377,476–101,377, and 554 on NCBI GRch37/hg19) were aligned using eBioX (http://www. [score:1]
To search for a homologous human gene in mouse Rian in the extended region, above 57-kb mouse genomic region (−14 kb to +43 kb) around miR-370 (110,856,468–110,856, and 546 on NCBI M37/mm9) were aligned approximately with human 168.5-kbp region encompassing a position −14 kb from miR-370 and miR-369 s (101,531,935–101,532, and 004 on NCBIGRch37/hg19) by using eBioX. [score:1]
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In the adult retina miR-124 and miR-125 were again prominent, but others, including miR-24, miR-326, miR-370, miR-96 and let-7 also had highly significant predicted effects. [score:1]
A range of other candidates with p-values < 0.05 in at least one experimental condition (miR-128, miR-150, miR-204, miR-25, miR-27, miR-326 miR-34, miR-370, miR-378 and miR-485-5p) were selected to represent different predicted patterns of activity or for their lack of previous association with neural tissue. [score:1]
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In addition, miRNAs have been described to be modulated even in steatosis/NASH (i. e. miR-155, miR-370, miR-34a, miR-200a/b, miR-99a/b), fibrosis (i. e. miR-200a/b, miR-221/222, miR-34a, miR-16, miR-99b), cirrhosis (i. e. miR-34a, miR-21, miR-31, miR-181b), and HCC (i. e. miR-16, miR-33, miR-21, miR-31, miR-181a/b, miR-99a, miR-200a/b) [15]. [score:1]
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Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-134, mmu-mir-136, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-379, mmu-mir-181b-2, rno-mir-21, rno-mir-127, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-431, mmu-mir-433, rno-mir-431, rno-mir-433, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
Other families that had a high abundance of reads were miR-134, miR-136, miR-154, miR-370, miR-412, miR-431, miR-432, miR-433, miR-485, miR-493, miR-541; a total of 11 miRNA families. [score:1]
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However, in sheep, the analyzed miRNA sites that are located in the 505 bp 3′ UTR of the ovine s-SCF (+) form belongs to the miRNA families of miR-27a/b, miR-194, miR-128, miR-370, and two sites for miR-132/212, miR-320/320abcd (Figure 9(a)) where as miR-669f/a/o-3p, miR-466b and miR828b are detected on the shorter 3′ UTR segment (144 bp) of ovine m-SCF (−) form (Figure 9(b)). [score:1]
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86 miR-873-as 1,016 e-miR-743b-5p 23.75 miR-449c-as 515e-miR-715 || 69.35 miR-541-as 439 e-miR-881* 56.21 miR-148b-as 336 e-miR-370 97.41 miR-546-as 333 e-miR-3067 100 miR-3074-as 262 e-miR-448-5p 100miR-451-as ‡ 286 e-miR-669o-5p 99.35 † Novel miR* that are processed within the expected window of the mature strand are labelled “generic”. [score:1]
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It has been demonstrated that miR-370 induces the accumulation of hepatic triglycerides through interacting with miR-122 and Cpt 1α [23]. [score:1]
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Comparing the operated knee with contralateral control showed two miRNAs increased by DMM surgery >1.5-fold at day 1 (miR-144-3p and miR-29b-3p) and two miRNAs at day 3 (miR-370-5p and miR-21-5p). [score:1]
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Other miRNAs from this paper: hsa-mir-370, hsa-mir-335, mmu-mir-335, mmu-mir-433, hsa-mir-433
One, rs47500792, is in a putative binding site for mmu-miR335-3p, and the other two, rs47154027 and rs46439487, are adjacent SNPs that are in a putative binding site for mmu-miR370. [score:1]
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