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82 publications mentioning mmu-mir-130b

Open access articles that are associated with the species Mus musculus and mention the gene name mir-130b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 275
Western blot analysis demonstrated that anti-miR-130b up-regulated the expression level of PPARγ but down-regulated VEGF-A and BCL-2. GW9662 abolished the effect of miR-130b inhibition on the expression of VEGF-A and BCL-2 (Fig.   6a). [score:13]
Fig. 8 Schematic diagram of microRNA-130b in promoting lung cancer progression via PPARγ/VEGF-A/BCL-2 -mediated suppression of apoptosis Studies have demonstrated that miR-130b suppresses migration and invasion of colorectal cancer cells through downregulation of Integrin-β1 [24]. [score:8]
In vitro and in vivo, miR-130b enrichment associated with down-regulation of PPARγ, up-regulation of VEGF-A and BCL-2, and decreased apoptosis. [score:7]
Functionally, our data indicate that miR-130b not only exhibits a potent oncogenic role, in agreement with other recent reports [30], but also suppresses lung cancer cell apoptosis through VEGF-A -mediated up-regulation of BCL-2, the classical anti-apoptotic gene. [score:6]
MiR-130b has also been documented in several other kinds of tumors, with up-regulation in melanoma [6], but down-regulation in endometrial cancer [7] and pituitary adenomas [8]. [score:6]
a Requirement of PPARγ in miR-130b mediated expressions of VEGF-A and BCL-2. b Bevacizumab down-regulated BCL-2 in a time- and c dose -dependent manner. [score:6]
However, in the context of gain-of-function p53 mutations, mutant p53 triggers EMT by indirectly inducing ZEB1 expression through negative regulation of miR-130b [27]. [score:6]
We demonstrate that miR-130b targets PPARγ and suppresses lung cancer cell apoptosis through the VEGF-A/BCL-2 pathway. [score:5]
Inhibition of miR-130b increased PPARγ expression but decreased VEGF-A and BCL-2 as confirmed by immunofluorescence microscopy (Fig.   3a and b). [score:5]
Notably, microRNA-130b targeted PPARγ and inhibiting microRNA-130b markedly repressed proliferation, invasion and metastasis of lung cancer cells, leading to increased apoptosis. [score:5]
In terms of the correlations between PPARγ, VEGF-A and apoptosis, we hypothesize that miR-130b suppresses PPARγ and promotes lung cancer progression via VEGF-A/BCL-2 -mediated inhibition of apoptosis. [score:5]
MiR-130b inhibitor (anti-M), miR-130b mimic, or the appropriate negative controls of miRNA inhibitor (anti-MC) and miRNA mimic were purchased from GenePharma (Shanghai, China). [score:5]
AD, adenocarcinoma; anti-M, anti-miR-130b; anti-MC, anti-miR-130b control; EMT, epithelial to mesenchymal transition; miR-130b, microRNA-130b; NL, normal lung; NSCLC, non-small-cell lung cancer; NT siRNA, non -targeting small interference RNA; PPARγ, peroxisome proliferator-activated receptor γ; PPRE, PPAR-response element; SD, standard deviation; SQ, squamous cell carcinoma; TUNEL, terminal deoxynucleotidyl transferase -mediated uridine 5’-triphosphate-biotin nick end labeling; VEGF-A, vascular endothelial growth factor-A; ZEB1, zinc finger E-box -binding homeobox 1 1:MiR-130b mimic enhances lung cancer cell aggressiveness via PPARγ/VEGF-A/BCL-2 -mediated suppression of apoptosis. [score:5]
We found that miR-130b, by targeting PPARγ, promotes aggressiveness through VEGF-A -mediated suppression of apoptosis in lung cancer. [score:5]
Studies have revealed that miR-130b promotes tumor aggressiveness by suppressing PPARγ but promotes VEGF-A expression and epithelial to mesenchymal transition (EMT) in hepatocellular [18] and colorectal cancer [5]. [score:5]
Immunoprecipitation analysis revealed that bevacizumab significantly inhibited the interaction between PPARγ and VEGF-A upon miR-130b inhibition (Fig.   6d), suggesting VEGF-A acted as the downstream of PPARγ in mediating the cascade of events. [score:5]
Another major finding of this study is that PPARγ antagonist GW9662 attenuates the effect of miR-130b inhibition on VEGF-A/BCL-2 -mediated apoptosis and downstream gene expressions. [score:5]
This is in line with other studies showing that miR-130b up-regulation correlates with the clinical stage of gastric [35] and esophageal carcinoma [30]. [score:4]
Moreover, varied expression levels of miR-130b have been found in endometrial [27], gastric [28] and bladder [29] cancer regulating different signaling molecules. [score:4]
Kaplan-Meier survival analysis demonstrated that patients with high miR-130b expression had a shorter overall survival time compared to patients with low miR-130b expression (Fig.   1e, 48.4 vs. [score:4]
Our results have revealed for the first time that miR-130b, through up -regulating the BCL-2 signaling, enhances lung cancer progression and inhibits cell apoptosis. [score:4]
It has been demonstrated that in wild-type p53 expressing cells, miR-130b directly represses Zinc finger E-box -binding homeobox 1 (ZEB1), opposing EMT and invasive phenotypes. [score:4]
These results demonstrated that VEGF-A silencing induced cell apoptosis via inhibition of BCL-2. However, VEGF-A had no feedback regulation on miR-130b in lung cancer cells. [score:4]
However, neither PPARγ nor VEGF-A siRNAs had feedback regulatory effects on the miR-130b expression. [score:4]
b MiR-130b expression in relation to the expression of PPARγ, VEGF-A and BCL-2. c Representative TMA sections stained for PPARγ, VEGF-A and BCL-2 by immunohistochemistry (scale bar, 100 μm), and apoptosis by (scale bar, 50 μm). [score:4]
Attenuation of the effect of miR-130b inhibition on apoptosis by GW9662. [score:3]
These data highlight the critical role of miR-130b in promoting lung cancer progression through PPARγ/VEGF-A/BCL-2 -mediated suppression of apoptosis (Fig.   8). [score:3]
MicroRNA-130b up-regulation conferred unfavorable prognosis of lung cancer patients. [score:3]
These results collectively suggested that miR-130b inhibition decreased lung cancer cell aggressiveness via PPARγ/VEGF-A/BCL-2 -mediated enhancement of apoptosis. [score:3]
By qRT-PCR (Fig.   1a), low level of miR-130b was detected in 46 cases and high miR-130b expression was found in 45 cases. [score:3]
However, PPARγ siRNAs had no effects on the expression level of miR-130b (Fig.   4l). [score:3]
MiR-130b up-regulation has been detected in lung adenocarcinoma and squamous cell carcinoma and confers advanced tumor stage, poor differentiation and unfavorable prognosis of lung cancer patients. [score:3]
However, we found that in lung cancer tissues, cases with high miR-130b expression level did not correlate positively with lymph node metastases and larger tumor size. [score:3]
Anti-MC: anti-miR-130b control; anti-M: anti-miR-130b; TUNEL, terminal deoxynucleotidyl transferase -mediated uridine 5’-triphosphate-biotin nick end labeling; UTR, untranslated region; wt, wild type; mt, mutant type. [score:3]
Targeting microRNA-130b might have remarkable therapeutic potential for lung cancer therapy. [score:3]
PPARγ antagonism abolishes the effect of miR-130b inhibition on VEGF-A/BCL-2 -mediated apoptosis. [score:3]
Flow cytometric analysis (Fig.   6f, upper panels) and the (Fig.   6f, middle panels) demonstrated that PPARγ antagonist GW9662 attenuated the effect of miR-130b inhibition on VEGF-A/BCL-2 -mediated apoptosis (Fig.   6f, lower panels). [score:3]
Our results have shown that miR-130b promotes lung cancer progression through PPARγ/VEGF-A/BCL-2 -mediated suppression of apoptosis. [score:3]
Fig. 6PPARγ antagonism dampens the effect of miR-130b inhibition on VEGF-A/BCL-2 -mediated apoptosis. [score:3]
High miR-130b expression confers unfavorable prognosis of lung cancer patients. [score:3]
These findings indicate clinical values of our study and that miR-130b is a potential new therapeutic target for lung cancer diagnosis and treatment. [score:3]
This suggests that miR-130b acts as the upstream of the PPARγ/VEGF-A axis in mediating apoptosis and downstream gene expressions. [score:3]
To investigate whether miR-130b expression predicts patients’ prognosis, we examined miR-130b expression in tissues of lung cancer patients. [score:3]
However, VEGF-A siRNAs had no effects on miR-130b expression (Fig.   5l). [score:3]
The mean value of miR-130b expression in tumor tissues was calibrated to the levels detected in normal control tissues. [score:3]
The relative expression of miR-130b was shown as fold difference relative to U6. [score:3]
The present study demonstrates that microRNA-130b promotes lung cancer progression via PPARγ/VEGF-A/BCL-2 -mediated suppression of apoptosis. [score:3]
The monolayer of cells was scratched with a 200 μL pipette tip to create a wound gap, and treated with miR-130b inhibitor, siRNAs of PPARγ or VEGF-A, and control (0.1 % DMSO) at indicated time points. [score:3]
These data confirmed the in vitro findings and further supported the notion that miR-130b promoted tumor growth and suppressed apoptosis via PPARγ/VEGF-A/BCL-2 signaling. [score:3]
Fig. 1High miR-130b expression confers unfavorable prognosis of lung cancer patients. [score:3]
Future studies exploring the significance of circulating miR-130b in lung cancer development and progression may provide possible evidences for early detection and screening of lung cancer risk factors. [score:2]
Taken together, these results suggested that PPARγ functioned as a critical regulator in miR-130b mediated lung cancer apoptosis through the VEGF-A/BCL-2 pathway. [score:2]
The level of microRNA-130b in relationship with the expression of PPARγ, VEGF-A, BCL-2 and apoptosis were analyzed in 91 lung cancer patient samples using immunohistochemistry and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay on tissue microarrays. [score:2]
Yu T, Cao R, Li S, Fu M, Ren L, Chen W, Zhu H, Zhan Q, Shi R. MiR-130b plays an oncogenic role by repressing PTEN expression in esophageal squamous cell carcinoma cells. [score:2]
Egawa H Jingushi K Hirono T Ueda Y Kitae K Nakata W Fujita K Uemura M Nonomura N Tsujikawa K The miR-130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTENSci Rep. [score:2]
We found increased miR-130b expression in lung cancer tissues compared with corresponding normal lungs. [score:2]
Undoubtedly, miR-130b exerts a critical function in regulating cell apoptotic processes. [score:2]
MiR-130b depletion inhibited the ability of cells to invade (Fig.   3g), migrate (Fig.   3h) and form colonies (Fig.   3i). [score:2]
These studies demonstrate that miR-130b plays a role in regulating tumor progression. [score:2]
MicroRNA-130b -dependent biologic effects were due to suppression of PPARγ that in turn activated BCL-2, the key mediator of anti-apoptosis. [score:2]
MiR-130b inhibition attenuates lung cancer cell aggressiveness via PPARγ/VEGF-A/BCL-2 -mediated enhancement of apoptosis. [score:2]
MiR-130b may promote hepatocellular carcinoma cell migration and invasion by inhibiting PPARγ and subsequently inducing EMT [18, 25]. [score:2]
Furthermore, immunoprecipitation demonstrates the interaction between PPARγ and VEGF-A, supporting the notion that miR-130b plays a critical role in regulating lung cancer cell aggressiveness and apoptosis through the PPARγ/VEGF-A axis. [score:2]
MiR-130b promotes tumor growth and suppresses apoptosis via PPARγ/VEGF-A/BCL-2 signaling in mouse xenografts. [score:2]
MiR-130b expression associated with differentiation (p = 0.002) and TNM stage (p = 0.025) of lung cancer patients (Table  4). [score:2]
However, PPARγ did not have feedback regulation on miR-130b. [score:2]
a MiR-130b expression in lung cancer tissues. [score:2]
MicroRNA-130b PPARγ BCL-2 Apoptosis NSCLC Several microRNAs (miRNAs), such as miR-21, miR-152, miR-148b and miR-208a, play critical roles in lung cancer progression through modulating growth, apoptosis, metastasis and invasion [1– 4]. [score:1]
Previous report [34] and our present results identify miR-130b as an important signature in lung cancer. [score:1]
g Decreased number of invaded cells with anti-miR-130b treatment (scale bar, 100 μm). [score:1]
A recent study has identified microRNA-130 (miR-130) as a contributor in mesenchymal differentiation, hypoxic response modulation and tumorigenesis in colorectal cancer [5]. [score:1]
Kaplan-Meier method and the log-rank test were used to evaluate the difference between high and low miR-130b expression subgroups and the overall survival curves were generated. [score:1]
h Shorter migrated distance in cells treated with anti-miR-130b at indicated time points. [score:1]
H520 cells transfected with 120 ng anti-miR-130b, VEGF-A siRNA or negative controls, followed by co-transfection with 30 ng of the wild-type or mutant 3'-UTR of the mRNA of PPARγ or BCL-2 using 0.45 μL of Fugene (Promega, Madison, WI). [score:1]
f Apoptosis was increased by anti-miR-130b but decreased by GW9662. [score:1]
k Increased apoptotic rate in cells treated with anti-miR-130b (scale bar, 50 μm). [score:1]
As shown, miR-130b depletion led to a significant increase in the luciferase activity of the wild-type reporter but not the mutant (Fig.   3e). [score:1]
Anti-M: anti-miR-130b; bev. [score:1]
revealed that miR-130b abrogation significantly enhanced apoptosis and caused 52.6 % increase in the apoptotic rate (Fig.   3k). [score:1]
i Decreased colonies in cells treated with anti-miR-130b at 48 hours time point. [score:1]
Repression of microRNA-130b by thyroid hormone enhances cell motility. [score:1]
In lung cancer tissues, high miR-130b level corresponded with low PPARγ, high VEGF-A and BCL-2, and decreased apoptosis (Figs.   1b, c and d). [score:1]
Western blot analysis demonstrated that anti-miR-130b increased the level of PPARγ by 65.2 % but decreased VEGF-A and BCL-2 by 60.8 % and 38.5 %, respectively (Fig.   3d). [score:1]
l No effect of PPARγ siRNAs on the level of miR-130b. [score:1]
b Representative images of A549 cells treated with anti-miR-130b and labeled for BCL-2 (green) (scale bar, 50 μm). [score:1]
Correlations between expressions of miR-130b and PPARγ, VEGF-A and BCL-2 and lung cancer patients’ clinical pathological characteristics were analyzed using two-sided Fisher’s Exact Test. [score:1]
The average value between 0.5 to 1.0 was regarded as miR-130b low and the value between 1.0 to 1.6 as miR-130b high. [score:1]
Anti-miR-130b caused a significant increase in the luciferase activity of wt 3'-UTR of PPARγ. [score:1]
Administration of microRNA-130b mimic to mouse xenografts promoted tumor growth. [score:1]
e A shorter overall survival time in patients with high miR-130b. [score:1]
Conversely, miR-130b mimic had the opposite effects (Additional file 1: Supplementary Figure). [score:1]
The mutant PPARγ binding site was generated in the complementary site for the seed region of miR-130b. [score:1]
We also investigated the correlation between miR-130b expression and lung cancer patient’s prognosis and survival. [score:1]
d Correlations between miR-130b level and PPARγ, VEGF-A, BCL-2 or apoptosis. [score:1]
c and d Anti-miR-130b increased PPARγ, but decreased VEGF-A and BCL-2. e MiR-130b and its putative binding sequence in the PPARγ 3'-UTR. [score:1]
NC: normal control; miR-NC: miR-130b control; miR-130bm: miR-130b mimic; TUNEL, terminal deoxynucleotidyl transferase -mediated uridine 5’-triphosphate-biotin nick end labeling. [score:1]
a Representative images of A549 cells treated with anti-miR-130b and co-labeled for PPARγ (green) and VEGF-A (red) (scale bar, 50 μm). [score:1]
Mechanisms of miR-130b/PPARγ -mediated apoptosis and lung cancer progression were also explored. [score:1]
l No effect of VEGF-A siRNAs on the level of miR-130b. [score:1]
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[+] score: 183
miR-130b expression was significantly increased in the epididymal fat after miR-130b-MV injection while the protein content of its target gene PPAR-γ was significantly suppressed, together with a significant up-regulation of the lipolysis genes, hormone sensitive lipase, monoglyceride lipase and leptin. [score:10]
In summary, this is the first in vivo study demonstrating that miR-130b-MV can be shuttled into the epididymal fat tissue to down-regulate PPAR-γ expression and to stimulate the expression of lipolysis genes. [score:8]
Moreover, GR, TNF-α, UCP-3, SCD-1, LDLR, and STAT3, in addition to PPAR-γ, are also predicted to be the target of miR-130b, yet the mRNA expression of these genes in the epididymal fat tissue was not affected by miR-130b-MV treatment. [score:5]
The mRNA expression of adipose triglyceride lipase (ATGL) tended to be higher (P = 0.07) in miR-130b-MV -injected mice while the mRNA expression of leptin receptor was not affected. [score:5]
i: mRNA expression of the miR-130b target genes. [score:5]
The HeLa-229 cell expresses very low level of miR-130b [27], so it was chosen to serve as a carrier host for the over -expression of exogenous miR-130b. [score:5]
In the present study, miR-130b-MV increased HSL, MGL and leptin mRNA expression, but did not influence FAS and ACC mRNA expression. [score:5]
miR-130b-MV increased miR-130b expression and suppressed PPAR-γ protein content in epididymal fat. [score:5]
The mRNA expression of the predicted target genes of miR-130b, including GR, TNF-α, UCP-3, SCD-1, LDLR, STAT3, and PPAR-γ (Fig.   3i), was detected and only PPAR-γ tended to be increased (P = 0.07, Fig.   3j) in miR-130b-MV group. [score:5]
j: mRNA expression of the miR-130b target gene PPAR-γ. [score:5]
Recently, we demonstrated that miR-130b can be packaged into MVs and delivered to the recipient primary cultured porcine adipocytes to reduce lipid accumulation in vitro by inhibiting PPAR-γ expression [27]. [score:5]
Fig. 3Epididymal fat deposition, miR-130b and its target gene PPAR-γ expression. [score:5]
k: Protein expression of miR-130b target gene PPAR-γ. [score:5]
However, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) mRNA expression was significantly up-regulated (P < 0.01) in miR-130b-MV -injected mice when compared with miR-SC-MV mice (Fig.   4). [score:5]
HeLa-229 cells were transfected with the miR-130b over -expression plasmid, while plasmid over -expressing miR-SC was also transfected to serve as a negative control. [score:5]
We show that miR-130b was delivered to the epididymal fat tissue and significantly decreased the fat deposition, which was associated with a significant down-regulation of PPAR-γ protein content and an activation of lipolytic genes. [score:4]
MV- delivery miR-130b PPAR-γ Lipolysis Epididymal fat deposition High-fat diet induced obese mice Obesity is a major risk factor for the development of type II diabetes (T2DM), cardiovascular diseases, and some types of cancer [1– 5]. [score:4]
For instance, miR-378a and miR-378b-3p were up-regulated significantly in the epididymal fat tissue of miR-130b-MV -injected mice. [score:4]
Moreover, miR-130b-MV injection increased the expression of miR-378a and miR-378-3p that are reported to participate in the regulation of fat deposition. [score:4]
HF-SC-MV groupMoreover, miR-130b-MV did not affect the mRNA expression of CCTTA enhancer binding protein-β (C/EBP-β), peroxisome proliferators-activated receptor-α (PPAR-α), sterol regulatory element -binding protein 1 (SREBP1), or the lipogenic enzymes, fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC). [score:4]
HF-SC-MV group Moreover, miR-130b-MV did not affect the mRNA expression of CCTTA enhancer binding protein-β (C/EBP-β), peroxisome proliferators-activated receptor-α (PPAR-α), sterol regulatory element -binding protein 1 (SREBP1), or the lipogenic enzymes, fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC). [score:4]
Injection of miR-130b-MV affected the expression of lipid metabolic genes in the epididymal fat of high-fat diet -induced obese mice (Fig.   4). [score:3]
Our results indicate that miR-130b-MV is able to reduce the epididymal fat deposition and partly restore glucose tolerance, through translational repression of PPAR-γ in a high-fat diet -induced obese mouse mo del. [score:3]
miR-130b was packaged into MV by HeLa-229 cells transfected to over-express exogenous miR-130b. [score:3]
It is noted that miR-130b-MV also altered the expression of other miRNAs related to fat deposition. [score:3]
We have shown previously that microvesicle (MV)- delivered miR-130b (miR-130b-MV) is able to target PPAR-γ and subsequently reduce the lipid accumulation in vitro. [score:3]
miR-130b-MV affected expression of other miRNAs involved in lipid metabolism in epididymal fat. [score:3]
Nevertheless, it remains unknown whether MV-shuttled miR-130b can modulate fat deposition through targeting PPAR-γ in vivo. [score:3]
h: Expression of miR-130b gene in the epididymal fat. [score:3]
Here we provide the evidence that miR-130b-MV injection was effective to decrease body weight and reduce epididymal fat deposition in high-fat diet -induced obese mice in vivo, at least partly through the translational repression of PPAR-γ. [score:3]
In our previous study, we demonstrated that miR-130b-MV was able to reduce the lipid deposition in porcine primary adipocytes in vitro by targeting PPAR-γ gene [27]. [score:3]
b: Gene expression of miR-130b in miR-130b-MV. [score:3]
Further studies may be directed to assess the cytotoxicity and the half-life of miR-130b-MV in the blood, so as to further contribute to the development of anti-obesity drugs for clinical application. [score:3]
miR-130b-MV affected mRNA expression of lipid metabolic genes in epididymal fat. [score:3]
The expression of miR-378a and miR-378b-3P was significantly increased (P < 0.05) in the epididymal fat of miR-130b-MV -injected mice when compared with miR-SC-MV -injected mice (Fig.   5). [score:2]
The phenotypic changes in body size and fat deposition are shown in Fig.   3c-e, which indicate obviously reduced body weight and the epididymal fat mass in mice treated with miR-130b-MV. [score:1]
The effects and the side-effects, if any, of prolonged treatment of miR-130b-MV remain unclear. [score:1]
Therefore, it is presumed that miR-130b-MV decreases fat deposition predominantly by enhanced lipolysis but not lipogenesis. [score:1]
However, the in vivo effect of miR-130b on fat deposition and glucose homeostasis remains unknown. [score:1]
miR-130b-MV reduced body weight and epididymal fat weight. [score:1]
MV-packaged miR-130b was isolated from the culture media through ultracentrifugation and was injected intravenously to the obese mice. [score:1]
miR-130b-MV injection significantly reduced body weight and epididymal fat weight and partly restored glucose tolerance. [score:1]
Future studies are required to test the half-life of MV-protected miR-130b. [score:1]
Cell culture, miR-130b transfection and microvesicle isolation. [score:1]
Therefore, in the present study, we tested anti-obesity efficacy of MV-packaged miR-130b on a high-fat diet -induced C57BL/6 mouse mo del. [score:1]
Precursors of miR-130b and miR-SC were produced by annealing the upstream and downstream (50 μmol/L each) miRNA precursor sequences (Table  1). [score:1]
Then, we divided the obese mice randomly into two groups: (1) the control group injected with miR-SC-MV (HF-SC-MV); (2) the treated group injected with miR-130b-MV (HF-130b-MV). [score:1]
The above results suggest that intravenous injection of miR-130b-MV partly restored the glucose tolerance caused by high-fat diet. [score:1]
We further investigated the down-stream molecular mechanisms underlying the miR-130b-MV -mediated inhibition in fat deposition. [score:1]
We delivered miR-130b-MV to assess the anti-obesity effect of miR-130b in vivo. [score:1]
MVs containing miR-130b and miR-SC were purified from the supernatant of transfected cells and RT-PCR verified the package of significantly higher levels of miR-130b in miR-130b-MV preparations (Fig.   3b). [score:1]
The obese C57BL/6 mice were injected via tail vein with miR-SC-MV or miR-130b-MV every other day for 10 days. [score:1]
HF-SC-MV group Quantitatively, miR-130b-MV significantly reduced the body weight (P < 0.01), the epididymal fat weight (P < 0.05) (Fig.   3f) and the muscle weight (P < 0.05), but not the liver weight. [score:1]
MD10% group To determine the effects of miR-130b-MV injection on the glucose tolerance, OGTT was performed (Fig.   2). [score:1]
HF, high fat; HF-SC-MV, high-fat diet -induced obese mice injected with miR-SC-MV; HF-130b-MV, high-fat diet -induced obese mice injected with miR-130b-MV; The values shown represent the means ± SEM, n = 12; * P < 0.05 vs. [score:1]
OGTT, oral glucose tolerance test; HF, high fat; HF-SC-MV, high-fat diet -induced obese mice injected with miR-SC-MV; HF-130b-MV, high-fat diet -induced obese mice injected with miR-130b-MV; The values shown represent the means ± SEM, n = 12; P < 0.01 vs. [score:1]
However, miR-130b-MV injection was conducted every other day for 10 days due to limited quantity of the miR-130b-MV preparations. [score:1]
In the present study, we inspected histologically the possible side effects of miR-130b-MV on other tissues, including liver, kidney, heart and spleen. [score:1]
Three-week-old C57BL/6 mice were fed a high-fat diet for 8 weeks and then intravenously injected with MV-packaged scrambled control microRNA (miRNA) or miR-130b every other day for 10 days. [score:1]
miR-130 has been shown to strongly reduce adipogenesis by repressing PPAR-γ biosynthesis in human primary preadipocytes and 3T3-L1 mouse adipocytes [17]. [score:1]
Our results provide the preliminary evidences that MV -mediated delivery of miR-130b is able to reduce fat deposition in a high-fat diet -induced obese mo del. [score:1]
The abundance of miR-130b in the epididymal fat tissue was significantly higher (P < 0.05) in HF-130b-MV group (Fig.   3h). [score:1]
The precursors of miR-130b (89 bp) and the negative control miRNA (Scrambled control, miR-SC) were synthesized by Life Technologies Inc. [score:1]
miR-130b-MV partly restored glucose tolerance. [score:1]
However, the protein content of PPAR-γ was significantly reduced (P < 0.05) in the epididymal fat of mice injected with miR-130b-MV (Fig.   3k). [score:1]
This indicates that the general metabolic homeostasis of the body was not disturbed by miR-130b-MV treatment. [score:1]
miR-130b-MV and miR-SC-MV preparations were injected via tail vein into the obese mice of treatment and control groups respectively every other day for 10 days. [score:1]
miR-130b-MV was harvested by transfecting HeLa-229 cells with miR-130b plasmid. [score:1]
HF-SC-MV groupQuantitatively, miR-130b-MV significantly reduced the body weight (P < 0.01), the epididymal fat weight (P < 0.05) (Fig.   3f) and the muscle weight (P < 0.05), but not the liver weight. [score:1]
When the cells reached 90-95 % confluence, plasmids of 50 μg miR-130b and 50 μg miR-SC were transfected separately with Lipofectamine 2000 (Life Technologies Inc. [score:1]
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[+] score: 33
The ten most up-regulated miRNAs included mmu-miR-205-5p, mmu-miR-222-3p, mmu-miR-205-3p, mmu-miR-146b-5p, mmu-miR-21-5p, mmu-miR-21-3p, mmu-miR-221-3p, mmu-miR-140-3p, mmu-miR-142-5p, and mmu-miR-140-5p and the ten most down-regulated miRNAs comprised mmu-miR-211-5p, mmu-miR-3096-5p, mmu-miR-711, mmu-miR-466h-5p, mmu-miR-130b-3p, mmu-miR-3082-5p, mmu-miR-1199-5p, mmu-miR-669b-5p, mmu-miR-1187, and mmu-miR-1224-5p (Table 1). [score:7]
Furthermore, we also identified several miRNAs, which were significantly down-regulated in curcumin -treated melanomas, such as mmu-miR-130b-3p. [score:4]
Taken together, these results indicate that the curcumin-regulated miRNAs mmu-miR-205-5p, mmu-miR-205-3p, mmu-miR-142-5p and mmu-miR-130b-3p represent promising targets as well as markers to determine the aggressiveness and metastatic activity of malignant tumors. [score:4]
To investigate whether the curcumin -induced expression pattern of the key miRNAs identified in the in vivo experiments is also transferable to other melanoma cell lines, murine B78H1 cells as well as human SK-MEL-28 (ATCC® HTB-72™) and MeWo cells (ATCC® HTB-65™) were treated with 20 µM curcumin or vehicle (0.1% DMSO; control) at 37°C and 5% CO [2] for 48 h. Subsequently, the cells were harvested and the expression of mmu-miR-205-5p, mmu-miR-205-3p (or hsa-miR-205-3p for human cells), mmu-miR-142-5p and mmu-miR-130b-3p was analyzed by qRT-PCR, as described above. [score:3]
For the validation of the miRNA microarray results, qRT-PCR was performed to analyze the expression of the four selected miRNAs mmu-miR-205-5p, mmu-miR-205-3p, mmu-miR-142-5p and mmu-miR-130b-3p using miScript PCR System (Qiagen). [score:3]
The expression levels of mmu-miR-205-5p, mmu-miR-205-3p, mmu-miR-142-5p and mmu-miR-130b-3p, which have previously been described in the literature as miRNAs with potential anti-cancer properties [37], [38], were confirmed by qRT-PCR (Figure 2). [score:3]
0081122.g002 Figure 2 The diagrams display bar charts on the fold expression (compared to control) of mmu-miR-205-5p, mmu-miR-205-3p, mmu-miR-142-5p and mmu-miR-130b-3p in curcumin -treated B78H1 melanoma, as assessed by miRNA array (grey bars) and qRT-PCR (black bars). [score:2]
0081122.g003 Figure 3 The diagram displays bar charts on the fold expression (compared to vehicle -treated control cells) of mmu-miR-205-5p, mmu-miR-205-3p, mmu-miR-142-5p and mmu-miR-130b-3p of curcumin -treated murine B78H1 (white bars), human SK-MEL-28 (grey bars) and human MeWo melanoma cells (black bars), as assessed by qRT-PCR. [score:2]
The diagrams display bar charts on the fold expression (compared to control) of mmu-miR-205-5p, mmu-miR-205-3p, mmu-miR-142-5p and mmu-miR-130b-3p in curcumin -treated B78H1 melanoma, as assessed by miRNA array (grey bars) and qRT-PCR (black bars). [score:2]
The diagram displays bar charts on the fold expression (compared to vehicle -treated control cells) of mmu-miR-205-5p, mmu-miR-205-3p, mmu-miR-142-5p and mmu-miR-130b-3p of curcumin -treated murine B78H1 (white bars), human SK-MEL-28 (grey bars) and human MeWo melanoma cells (black bars), as assessed by qRT-PCR. [score:2]
Li et al. [45] could demonstrate that hsa-miR-130b induces epithelial-to-mesenchymal transition in endometrial cancer. [score:1]
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[+] score: 28
MiRanda and TargetScan predicted SOCS1 as the target gene of miR-142-5p, while all three miRNA target prediction databases predicted PPARγ as the target gene of miR-130-3p. [score:9]
Furthermore, silencing HDAC2 in M(IL-4) increased histone acetylation at the miR-130 promoter and miR-130a-3p expression (Fig. 8j,k), suggesting that IL-4 induces histone deacetylation of the miR-130a promoter by enhancing HDAC2 expression. [score:5]
PPARγ elevation in M(IL4) was inhibited by rescuing miR-130-3p expression with miRNA mimics, but was retrieved by co-transfection with PPARγ-mut carrying a mutated miR-130-3p seed sequence at its 3′ UTR, but not with a wild-type PPARγ vector (Fig. 5d). [score:5]
We further determined whether elevated PPARγ expression due to reduced miR-130-3p expression contributes to M2 polarization in M(IL4). [score:5]
Moreover, recovering PPARγ expression in M(IL-4) that were transfected with miR-130-3p mimics retrieved M2 polarization (Fig. 5e) and the profibrogenic effects of the macrophages (Fig. 5f). [score:3]
Then, the sections were hybridized with 20 nM 5' digoxigenin -labelled LNA control probe and miR-142-5p or miR-130-3p probe (Exiqon) overnight at 42 °C, then rinsed twice with 5 × SSC at room temperature, washed three times in 2 × SSC/50% formamide at hybridization temperature for 20 min and washed four times in PBS with 0.1% Tween 20 (PBST). [score:1]
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[+] score: 25
Lee E. K. Lee M. J. Ab delmohsen K. Kim W. Kim M. M. Srikantan S. Martindale J. L. Hutchison E. R. Kim H. H. Marasa B. S. miR-130 Suppresses Adipogenesis by Inhibiting Peroxisome Proliferator-Activated Receptor γ Expression Mol. [score:7]
These include the miR-130 family members that repress brown and white adipogenesis via direct inhibition of Pparg [30] and miR-378 that activates Cebpa and Cebpb expression during adipogenesis and enhances brown fat expansion [31, 32]. [score:6]
Expression of miR-130 is increased in adipocyte hypertrophy and fat inflammation [41] and interestingly, miR-130 of the current Fto- KO BAT was significantly decreased in comparison with WT, indicating a role for FTO in the regulation of miR-130 and the pathophysiology of obesity. [score:4]
PPARγ and C/EBPβ are important transcription factors in both brown and white adipogenesis and are inhibited by miR-130 and miR-155, respectively [30, 33]. [score:3]
Expression of miR-130b, a repressor of Pparg [30], was decreased 1.7-fold in Fto- KO mice compared with WT irrespective of the diet (Figure 2). [score:2]
Kim C. Lee H. Cho Y. M. Kwon O. J. Kim W. Lee E. K. TNFα-Induced miR-130 Resulted in Adipocyte Dysfunction during Obesity-Related Inflammation FEBS Lett. [score:1]
Furthermore, HFD induced a 2.3-fold increase in miR-130b, a repressor of Pparg [30], in the scWAT of WT mice but not in Fto- KO mice. [score:1]
In addition, miR-130 was reported to be increased in WAT of mice due to HFD [41], which was also observed in our WT mice but not in the Fto- KO mice. [score:1]
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[+] score: 18
Seven conserved DE miRs are upregulated during pneumonia and are expressed at moderate to high levels in lung neutrophils (average normalized mean expression above 5): mmu-miR-1224-5p, mmu-miR-188-5p, mmu-miR-139-5p, mmu-miR-15b-5p, mmu-miR-721, mmu-miR-18a-5p, and mmu-miR-130b-3p. [score:8]
We identified a network containing seven upregulated conserved miRs (mmu-miR-1224-5p, mmu-miR-188-5p, mmu-miR-139-5p, mmu-miR-15b-5p, mmu-miR-721, mmu-miR-18a-5p and mmu-miR-130b-3p) and another network consisting of downregulated miRs belonging to 3 highly conserved miR families (let-7, mir-30 and mir-34). [score:7]
Two of these, mmu-miR-721 and mmu-miR-130b-3p, belong to the same broadly conserved miR family and are therefore predicted to share target mRNAs in common. [score:3]
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[+] score: 17
The results showed that 5 miRNAs (miR-130b-5p (formerly designated as miR-130b*), miR-196a, miR-455-3p, miR-455-5p, and miR-801) or 2 miRNAs (miR-133b and miR-145) were significantly up-regulated or down-regulated, respectively in laryngeal cancers (Figure 1A). [score:7]
While miR-130b-5p, miR-455-3p, miR-455-5p, and miR-801 were up-regulated in laryngeal cancer in our study, much less study has been performed on these miRNAs before. [score:4]
miR-130b-3p complementary to miR-130b-5p was reported to be related to schizophrenia by targeting MECP2 protein [58]. [score:3]
Higher expression levels of miR-130b-5p were observed in cancer tissues compared with neighboring controls in 4 of 5 pairs. [score:2]
Thus, qRT-PCR analysis was performed on residual 4 miRNAs (i. e., miR-130b-5p, miR-196a, miR-455-5p, and miR-133b). [score:1]
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[+] score: 16
Furthermore, qPCR was performed again to validate the downregulated and upregulated expression of selected miRNAs that may be relevant to development and confirmed that miR-135, miR-302, miR-449a, miR-200b, miR-200c, miR-193b, miR-130, and miR-141 were downregulated, whereas miR-10a, miR-181, and miR-470 were upregulated by RA treatment (Fig 4C and 4D). [score:16]
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[+] score: 15
As shown in Figure 6B, the CREB transcriptional targets AREG, Cyclin A and miR-130b showed an upregulated profile, whereas miR-1 appeared downregulated in Ccdc6 [−ex2/−ex2] mice with respect to the Ccdc6 [wt/wt] mice. [score:9]
In order to investigate whether the increase in the phosphorylation status may reflect the transcriptional ability of the thyroid cells, we have analysed the levels of some CREB1 target genes, such as AREG, Cyclin A, miR-130b (positively regulated by CREB1) and miR-1 (negatively regulated by CREB1) in hyperplastic thyroids of Ccdc6 [−ex2/−ex2] mice and controls. [score:3]
B. AREG, CCNA2, miR-1 and miR-130b genes expression by qRT-PCR from Ccdc6 [wt/wt] and Ccdc6 [−ex2/−ex2] thyroids. [score:3]
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[+] score: 13
The predicted sites for miR-130 and miR-17/20 within the Cd69 3' UTR also affected eGFP reporter gene expression in DP thymocytes. [score:3]
However, deletion of the miR-130 and particularly the miR-17/20 site resulted in increased eGFP expression in wild type CD4+ T cells (Fig. 3C). [score:3]
A dual fluorescence reporter system identifies endogenous microRNAs that target the Cd69 3'UTR in DP thymocytesThe Cd69 3'UTR contains predicted sites for miR-181, miR-130 and miR-17/20 (http://www. [score:3]
org) and there is firm experimental evidence for Cd69 regulation by miR-181a, miR-130 and the miR-17-92 cluster (which encodes the microRNAs miR-17, -18, -19a, -19b, -20a, and -92 [34] in T lymphocytes [31– 33]. [score:2]
The Cd69 3'UTR contains predicted sites for miR-181, miR-130 and miR-17/20 (http://www. [score:1]
The 842 nt 3’ UTR of Cd69 contains predicted binding sites for miR-181, miR-130 and miR-17-20 starting at positions 255, 354 and 391, respectively, which were mutated alone and in combination. [score:1]
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[+] score: 12
Similar observation was also derived for eQTL mapped (peak SNP, rs6413270) for miR-130b where minor allele (BB) derived for MRL/MpJ and NZM/2410J was associated with lower expression of miR-130b, and late onset of disease phenotype (Fig.   5a). [score:5]
The eQTL for miR130b (Chr 9: 36–44 Mb, −log P = 4.42), miR-542-3p (Chr 12: 79–103 Mb, −log P = 4.73) and miR-449b (Chr 14: 50–72 Mb, −log P = 4.49) were mapped on QTL for disease onset on chromosome 9, 12 and 14. [score:3]
The variation associated with three genotypes AA, AB and BB for expression of miR-130b is presented on left and onset week of EBA on right box. [score:3]
a) In miR-130b eQTL, peak SNP (rs6413270, −logP = 4.22) have genotype AA for BxD2 and CAST/EiJ while BB for NZM/2410J and MRL/MpJ strain. [score:1]
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[+] score: 11
In CD133 [+] HCC cells, miR-130b was overexpressed and enhanced chemoresistance, tumorigenicity and self-renewal [18], whereas miR-150 was down-regulated and significantly inhibited tumor sphere formation and cell growth [30]. [score:8]
To date, in HCC, miR-130b has been shown to promote CD133 [+] CSC tumorigenicity and self-renewal [18], whereas miR-181 inhibition reduces the number of EpCAM [+] CSCs and tumor-initiating ability [19]. [score:3]
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[+] score: 11
miR-27a and miR-130 suppress adipogenesis by inhibiting PPARγ (Kajimoto et al, 2006), whereas miR-143 induces adipogenesis by downregulating ERK5 (Esau et al, 2004). [score:8]
Several miRNAs, including miR-27a, miR-130 and miR-143, were previously shown to regulate adipogenesis. [score:2]
Recently, miRNAs in adipocytes have been shown to alter cell proliferation (the miR-24-1, miR-31 and miR-17-92 cluster) (Sun et al, 2009; Wang et al, 2008), repress Wnt signalling (miR-8) (Kennell et al, 2008), or repress peroxisome proliferator-activated receptor γ (PPARγ; miR-27a, miR-27b and miR-130) (Karbiener et al, 2009; Kim et al, 2010; Lin et al, 2009). [score:1]
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[+] score: 10
Of the eight differentially expressed miRNAs found in both males and females exposed to O [3], a total of six miRNAs were upregulated exclusively in males: miR-338-5p (log fold change = 1.636), miR-222-3p (log fold change = 0.699), miR-130b-3p (log fold change = 0.646), let-7i-5p (log fold change = 0.552), miR-195a-5p (log fold change = 0.543), and miR-144-3p (log fold change = 0.427) (Fig.   2). [score:6]
Several of these were also involved in inflammation (miR-130b-3p, miR-17-5p, miR-294a-3p, and miR-338-5p) and targeted key regulators of the immune response including IL-6, SMAD2/3, and TMEM9 (Table  1, Additional file  3: Figure S2B). [score:4]
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[+] score: 10
Additionally, we detected upregulated miRNAs targeting important tumor suppressor genes in diverse neoplasia, such as miR-638 (BRCA1), miR-130b (TP53), miR-130b (CSF1), miR-142-3p (IL1A), and miR-301a (BIM, PTEN) (Table 2). [score:8]
showed that expression levels of miR-335, miR-10b, miR-944, miR-301a, miR-18b, miR-204, miR-130b, and miR-188-5p were similar in both assays (Fig. 1B). [score:2]
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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-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-214, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-141, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-96, hsa-mir-200c, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-200a, hsa-mir-130b, hsa-mir-376a-1, mmu-mir-376a, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, hsa-mir-429, mmu-mir-429, hsa-mir-450a-1, mmu-mir-450a-1, dre-mir-429a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-130b, dre-mir-141, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, hsa-mir-450a-2, dre-let-7j, hsa-mir-376a-2, mmu-mir-450a-2, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
We found eight miRs differentially expressed, six down-regulated (miR-9, miR-141, miR-200a, miR-200b, miR-429 and miR-376a) and two up-regulated (miR-450a-5p and miR130b*) in the Dlx5 [−/−] OE (Fig.  1a). [score:9]
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[+] score: 9
Statistical data analysis revealed that the mean expression level of 9 miRNAs (i. e. ; miR-128, miR-99b-5p, miR-130b-3p, miR-142-3p, miR-374a-5p, miR-423-5p, miR-484, miR-629-5p, let-7d-3p) was significantly different (student t-test p<0.05) across the studied groups (Table 2). [score:3]
Considering the whole population, this analysis revealed 4 differentially expressed miRNAs (miR-128, miR-130b-3p, miR-374a-5p, miR-423-5p) in subjects with prediabetes and T2DM patients compared to control subjects with normal glucose tolerance. [score:2]
In the context of the well-known insulin-resistance effects, high-fat diet led to increased circulating concentrations of miR-128, miR-130b-3p, miR-99b-5p, miR-629a-5p and miR-let-7d-3p expression in HFD mice compared with NPD fed mice (p<0.05). [score:2]
In addition, miR-374a-5p and miR-130b-3p were altered in the same direction in the whole group of patients suffering from T2DM than in discovery group, compared to the control group of subjects, and miR-130b-3p was only affected in the T2DM group. [score:1]
2012-1996 31 Wang Y-cC, Li Y, Wang X-yY, Zhang D, Zhang H, Wu Q, et al Circulating miR-130b mediates metabolic crosstalk between fat and muscle in overweight/obesity. [score:1]
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[+] score: 9
As discussed, p73 may inhibit the expression of ER-α through its ability to increase the processing of miR-130b/181d. [score:5]
Thus, p73, by increasing the expression of Ago-1/2, it could increase the processing of miRNAs, such as let-7 (HMGA2; lin-28; EGFR; Kras; c-myc; Bcl-xL), miR-134 (Nanog; LRH1; Oct-4; Collagenase-3; Stromelysin), miR-130b (ERK2; Fosl1; TGFβR1; ERα; Tcf-4; Collagenase-3; Ago4; Dicer; p63), miR-214 (EZH2; CTNNB1), miR-449a (CDK6; SirT1; HDAC1; E2F-1), miR-503 (CCND1; Fosl1), miR-181d (ERK2; TGFβR1; Tcl-1; ERα; AID; Bcl-2) and miR-379 (lin-28) [Figure 2] [31], [32]. [score:3]
The C-terminal NHL domain of TRIM-32 forms complex with Ago1, and thereby promotes the efficiency of processing of a number of miRNAs [Figure 2], including let-7, miR-134, miR-130, miR-214, 449, 379, 181, and miR-503 [31]. [score:1]
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[+] score: 9
Other miRNAs from this paper: mmu-mir-150
MiR-130b preferentially up-regulated in the CD133 [+] liver CSC cells via suppression of 53-inducible protein 1 [7], while miR-150 reduces CD133 [+] cells through downregulation of c-Myb proteins in HCC cells [22]. [score:9]
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[+] score: 9
Inhibition of FGF signaling through SU5402 -treated primitive streak regions of chick embryos identified up-regulation of let-7b, miR-9, miR-19b, miR-107, miR-130b, miR-148a, miR-203, and miR-218 and down-regulation of miR-29a and miR-489 (Bobbs et al. 2012). [score:9]
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[+] score: 8
Reexpression of both Dicer and miR130b in TAp63(−/−) MEFs decreased invasiveness of these cells, suggesting that TAp63's tumor suppressor role could be mediated at least in part through Dicer and miR130b [123]. [score:5]
As mentioned previously, miR130b targets ΔNp63 α for degradation [83]. [score:3]
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[+] score: 8
Apart from global modulation of miRNA biogenesis, mutant p53 also affects expression of miRNAs, principally by downregulating tumor-suppressive miRNAs – miR-130b in endometrial cancer (24), miR-27a in breast cancer cells (MDA-MB-468) (25), miR-223 in breast and colon cells (26), let-7i in breast cancer and DLD1 cells (colorectal cancer) (27), and miR-205 (28), and elevating oncogenic miRNAs: miR-128-2 (29) and miR-155 in breast cancer cells (30) to mediate its oncogenic functions. [score:8]
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[+] score: 7
In fact, miRNAs which are direct transcriptional targets of TAp63, miR-130b [26] and let-7i [17] have been shown to be downregulated by mutant TP53. [score:7]
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[+] score: 7
miR-130b was also up-regulated in human T-cell leukemia virus 1 (HTLV-1) -mediated cellular transformation [46]. [score:4]
miR-130b +miR-130b showed increased expression in patients with primary WHO grade II gliomas that spontaneously progressed to WHO grade IV secondary glioblastomas [45]. [score:3]
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[+] score: 7
Leone V. Langella C. Esposito F. De Martino M. Decaussin-Petrucci M. Chiappetta G. Bianco A. Fusco A. miR-130b-3p Upregulation Contributes to the Development of Thyroid Adenomas Targeting CCDC6 GeneEur. [score:7]
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[+] score: 7
Other miRNAs from this paper: mmu-mir-21a, mmu-mir-21b, mmu-mir-21c
Expression of miRNA130b, which targets STAT3, inhibits pancreatic cancer cell proliferation [53]. [score:7]
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[+] score: 7
Downregulation of the miR-130b–301b cluster impairs cellular senescence in prostate cancer [29], while miR-494-3p increases the radiosensitivity of oral squamous cell carcinoma cells through the induction of cellular senescence caused by the downregulation of Bmi1 [30]. [score:7]
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[+] score: 6
Maves et al. (2007) Development 134:3371–3382 miR-130b PPARγMultiple adipocyte genes, PPAR→ UCP1→ NRF1 Suppression of adipogenic differentiation in favour of osteogenesis or chondrogenesis. [score:4]
PPARγ (peroxisome proliferator-activated receptor γ) is potentially regulated by miR-130b that came up when comparing the between osteoblasts and chondroblasts. [score:2]
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[+] score: 6
For example, the functions of miR-130b, -708, -199a in VSMCs are completely unknown, although they were highly expressed in VSMCs and downregulated in Drosha c KO mutant embryos based on miRNA array data. [score:6]
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[+] score: 6
Interestingly, in our studies IBD -associated microRNA-130, -195, -196, -223, -375 were down-regulated in Tregs or naive T-cells after isotretinoin treatment, indicating that isotretinoin does not induce a microRNA expression pattern similar to the one observed in IBD patients. [score:6]
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[+] score: 6
Microarray analysis showed altered expression of some miRNAs in hepatomas such as let-7a, miR-21, miR-23, miR-130, whereas the hepato-specific miR-122a and others were found downregulated in 70% of HCCs and in HCC-derived cell lines [20], [46], [47], as reported in our data (Table 1). [score:6]
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[+] score: 6
Other miRNAs from this paper: mmu-mir-143, hsa-mir-143, hsa-mir-130b
Zhou D Cytidine monophosphate kinase is inhibited by the TGF-beta signalling pathway through the upregulation of miR-130b-3p in human epithelial ovarian cancerCell Signal. [score:6]
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[+] score: 5
Collectively, our results confirm the cornea expression of miRNAs already reported in literature [27, 31, 32] and reveal the corneal-enrichment of others that had not been previously described to be expressed in the eye (e. g. miR-130a, miR-130b, miR-132, miR-129-3p, the miR-200 family, miR-468, miR-874). [score:5]
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[+] score: 5
To validate miRNA targets, approximately 10 [5] 293T cells per well in a 24-well plate were transiently transfected with 0.3μg of each firefly luciferase reporter construct, 0.1μg of Renilla luciferase TK vector, and 0.6μg of pMSCV-miR-128-2 or control vector of pMSCV-miR-130 or pMSCV-miR-29b2. [score:3]
Plasmids encoding miR-130 or miR-29b2 preserved in our laboratory were used as controls. [score:1]
The plasmids pMSCV_GW_RfA_PGK_EGFP-miR-128-2, pMSCV_GW_RfA_PGK_EGFP-miR-130, and pMSCV_GW_RfA_PGK_EGFP-miR-29b2 (hereafter called pMSCV-miR-128-2, pMSCV-miR-130, and pMSCV-miR-29b2, respectively) encoding mature miR-128-2, miR-130, and miR-29b2, respectively, were provided by Dr. [score:1]
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[+] score: 5
Relevant to polyQ-ATXN1 cytotoxicity, Lee et al. found that ATXN1 levels might be post-transcriptionally regulated by miRNA, specifically miR-19, miR-101, and miR-130. [score:2]
miR-19, miR-101 and miR-130 co-regulate ATXN1 levels to potentially modulate SCA1 pathogenesis. [score:2]
When miR-19, miR101, and miR130 were transfected into HEK293T, HeLa and MCF7 cells, a marked decrease in ATXN1 levels was observed. [score:1]
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[+] score: 5
However, treatment with siADAM8-1 led to reduced levels of only eight miRNAs (miR-181a-2, miR-29c, miR-29c*, miR-98, miR-520c-3p, miR-93, miR-130b, and miR-720), whereas three miRNAs showed increased expression, including miR-30d, miR-20a and miR-106*b (Fig.   1d), suggesting these miRNAs may not be regulated specifically by ADAM8 or may have differential regulation via splice variants. [score:5]
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[+] score: 5
Other miRNAs from this paper: mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-130a, mmu-mir-186, mmu-mir-200b, mmu-mir-202, mmu-mir-30e, mmu-let-7d, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-192, mmu-mir-200a, mmu-mir-15a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-19a, mmu-mir-200c, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-466a, mmu-mir-467a-1, mmu-mir-669a-1, mmu-mir-669b, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-467b, mmu-mir-669c, mmu-mir-709, 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-467c, mmu-mir-467d, mmu-mir-574, mmu-mir-466d, mmu-mir-467e, mmu-mir-466l, mmu-mir-669k, mmu-mir-669g, mmu-mir-669d, mmu-mir-466i, mmu-mir-669j, mmu-mir-669f, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-669e, mmu-mir-467g, mmu-mir-467h, mmu-mir-669l, mmu-mir-669m-1, mmu-mir-669m-2, mmu-mir-669o, mmu-mir-669n, mmu-mir-466m, mmu-mir-669d-2, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-669p-1, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-466b-6, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-669p-2, 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-466p, mmu-mir-466n, mmu-mir-466b-8, mmu-mir-466q, mmu-mir-21b, mmu-mir-130c, mmu-mir-21c, mmu-mir-30f, mmu-mir-466c-3
Also, several microRNAs, such as miR-130, miR-192 and miR-200, have been reported to have a regulatory role in kidney diseases [16, 17]. [score:4]
In addition, let-7d-3p [20], miR-21[21], miR-29 [22], miR-30 [23], miR-130 [16], miR-192 [24], miR-200 [25, 26] have been reported to be related to kidney fibrosis. [score:1]
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[+] score: 5
Other miRNAs from this paper: mmu-mir-132
Those differentially expressed miRNAs with a fold-change > 2 and those with roles known to be associated with obesity, nonalcoholic fatty liver disease, and adipogenesis (e. g., mmu-miR-130b and mmu-miR-132) are shown in, Table S7. [score:5]
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Specifically, in TNFα -treated adipocytes, miR-146b, miR-130 and miR-155 were upregulated. [score:4]
Several miRNAs, such as miR-132 [15], miR-155 [16], miR-130 [17], miR-145 [18], miR-146b [19], and miR-29 [20] have been indentified in obesity -associated inflammation and insulin-resistance in adipocytes. [score:1]
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[+] score: 5
Other miRNAs from this paper: mmu-mir-126a, mmu-mir-126b
Microvesicle-shuttled mir-130b reduces fat deposition in recipient primary cultured porcine adipocytes by inhibiting PPAR-γ expression. [score:5]
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[+] score: 5
In fact, this same pattern of regulation was observed for other seven miRNAs (mmu-miR-29c, mmu-miR-296, mmu-miR-130b, mmu-miR-17, mmu-miR-434, mmu-miR-181c, mmu-miR-132), which further confirms the validity of our analysis and suggests miRNA regulation at the gene expression level [48]. [score:5]
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[+] score: 4
With respect to miRNAs which may regulate the expression of TP53INP1, several studies had reported that TP53INP1 was repressed by miR-155 in pancreatic cancer [32] and miR-130b in hepatocelluar cancer [37], respectively. [score:4]
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[+] score: 4
This could explain why miR-15b and miR-130 (down-regulated in HCC tissues in contrast to miR-15b) could be used as a set of highly accurate markers for HBV-related HCC (16). [score:4]
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[+] score: 4
As members of miR-130/301 family, miR-130a and miR-301a have been shown to be modulated by distinct transcriptional events (42) and are highly conserved for the 3′UTR of TNF-α among vertebrate as we observed that miR-130a-3p and -301a-3p mimics could downregulate TNF-α protein levels and reporter gene levels in both PAMs and RAW264.7 cells. [score:4]
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Epigenetic silencing of miR-130b in ovarian cancer promotes the development of multidrug resistance by targeting colony-stimulating factor 1. Gynecol. [score:4]
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[+] score: 4
Additional data indicate that FGF and BMP signaling pathway interactions are regulated by negative feedback loops involving microRNAs, particularly miR-130 and miR-133 [48, 49]. [score:2]
Lopez-Sanchez C. Franco D. Bonet F. Garcia-Lopez V. Aranega A. Garcia-Martinez V. Negative fgf8-bmp2 feed-back is regulated by mir-130 during early cardiac specification Dev. [score:2]
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[+] score: 4
A recent study has demonstrated that miR-130 family negatively regulates PTEN protein expression in bladder cancer cells 34. [score:4]
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a Box-plots of miRNA expression levels of mmu-miR-18a-5p, mmu-miR-31-5p, mmu-miR-130b-3p, mmu-miR-199a-5p, mmu-miR-200c-3p, mmu-miR-224-5p in mouse quadriceps muscle at 2 days, 2 weeks, 4 weeks and 12 weeks after birth. [score:3]
The top-ranked miRNAs for clusters A were mmu-miR-18a-5p, mmu–miR-31–5p, mmu-miR-130b–5p, mmu-miR-199a–5p, mmu-miR-200c–5p and mmu-miR-224–5p. [score:1]
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Since we previously showed that let-7 family (lin28 -mediated) 35 and miR-130b 44 were downregulated under diabetic conditions by mechanisms not involving p-MeCP2, we focused on miR-25 in this study. [score:4]
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Analysis of miR-4295, miR-301a, miR-301b, miR-130a, miR-130b, miR-454, and miR-3666 expression were carried out using the miScript PCR system (QIAGEN, Valencia, CA) by 7900HT Fast Real-time PCR system (Applied Biosystems, Foster City, CA). [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-296, mmu-mir-298, mmu-mir-34c, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, hsa-mir-330, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-519d, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-501, mmu-mir-718, mmu-mir-18b, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Our results are also mostly in agreement with those of Esau et al. [25] who identified a similar expression pattern regarding miR-130b, miR-30c, miR-30a*, miR-191, miR-30d, miR-196, miR-30b, miR-19b, miR-92, miR-138 and miR-100 during differentiation of cultured human adipocytes. [score:3]
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[+] score: 3
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-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, 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-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The miRNA families that change expression in both mice and rats were: mir-7, mir-9, mir-10, mir-15, mir-17, mir-26, mir-29, mir-30, mir-101, mir-130, mir-181, mir-204, mir-339, mir-340, mir-368, mir-434, mir-467. [score:3]
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[+] score: 3
Specific miRNAs that enhance adipocyte differentiation (miR-30c, miR-143, miR-146b, and miR-378; [21– 24]) or inhibit adipocyte differentiation (miR-27, miR-130, and miR-138; [25– 27]) have been identified. [score:3]
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They observed enhanced levels of miR-21 and miR-130 in venous ulcers patients, which delay healing of human wounds by targeting leptin receptor (LepR) [13]. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-130b
TAp63 isoforms suppress metastasis through induction of senescence [14] and transcriptional activation of Dicer1 and mir-130b, providing support for the metastatic phenotype associated with cells lacking TAp63[13]. [score:3]
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A statistically significant effect of flutamide was observed for seven of these miRNAs (miR-26b-3p, let-7b-3p, miR-465c-3p, miR-669h-3p, miR-3058-5p, miR-146b, miR-1843-5p), and a trend toward a statistically significant effect was observed for another miRNA (miR-130b-5p) (Fig.   2b, c). [score:1]
Eleven miRNAs were randomly selected for qPCR analysis for each age: GD 17.0 miR-1843-5p, miR-485-3p, miR-711, miR-3962, miR-3067-3p, miR-212-3p, miR-669i, miR-877, miR-26b-3p, miR-465c-3p, let-7b-3p; GD 18.0 miR-1843-5p, miR-485-3p, miR-3473d, miR-132-5p, miR-3074-1-3p, miR-128-2-5p, miR-130b-5p, miR-490-5p, miR-669h-3p, miR-3058-5p, miR-146b. [score:1]
The seven miRNAs presenting a statistically significant effect of flutamide and miR-130b-5p were used to compare qPCR and microarray data. [score:1]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-128-1, mmu-mir-98, mmu-mir-338, mmu-mir-128-2
Some examples in the literature are reported for other integrins, such as TGF-β, which acts through miR-130b to increase integrin alpha 5 expression and promote migration [84]. [score:3]
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[+] score: 3
Seven miRNAs (miR-31, miR-95, miR-99a, miR-130b, miR-10a, miR-134, and miR-146a) were expressed at 6-fold lower level in SLE patients than that of healthy controls (Tang et al., 2009). [score:3]
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[+] score: 3
miR-431, miR-714, miR-744, miR-877, miR-130b, miR-21, miR-323-3p, miR-325, miR-409-3p, miR-154*, and miR-681 were significantly increased 4 days post-sciatic nerve crush in pre-conditioned DRGs, while miR-190, miR-1, miR-33, miR-32, miR-153, miR-335-5p, miR-193, and miR-488 showed significantly decreased expression. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-130b, hsa-mir-1468, hsa-mir-1469
Our previous study confirms that miR-130b promotes cell aggressiveness by inhibiting PPAR-γ in human HCC [23]. [score:3]
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[+] score: 3
Yu et al. suggested that miR-130b plays an oncogenic role by repressing PTEN expression in esophageal squamous cell carcinoma cells [22]. [score:3]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-130a, mmu-mir-221, mmu-mir-130c
In contrast, miR-130 is pro-angiogenic, promoting endothelial cell proliferation and migration by inhibiting anti-angiogenic homeobox proteins [13]. [score:3]
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Elevated miR-130a/miR130b/miR-152 expression reduces intracellular ATP levels in the pancreatic beta cell. [score:3]
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The miRNAs that contributed most prominently to PC1 (human - mouse split) were miR-93 and miR-19a, with a lesser contribution from miR-19b, miR-20a and miR-130b, while the miRNAs that contributed most significantly to PC2 (MYCN high versus low expression) were miR-17, miR-25, miR-20b and miR-15b. [score:3]
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For example, we found that the expression of 3 miRNA (mmu-miR-130b-3p, mmu-miR-135a-5p, mmu-miR-692) displayed no differences between tumor and parenchyma in the absence of cigarette smoke exposure and therefore their interaction statistics reflected exclusively the effects of exposure. [score:3]
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Interestingly, palbociclib also reduced expression of two other miRNAs elevated in PN GBM, miR-130b (in both G44 and G559 PN GSC lines) and miR-10b (in G559 PN GSC line). [score:3]
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[+] score: 2
miR-19, miR-101 and miR-130 co-regulate ATXN1 levels to potentially modulate SCA1 pathogenesis. [score:2]
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[+] score: 2
For instance, miR-142-5p plays critical roles in lymphocyte development and homeostasis (57), and miR-106a-5p, miR-130-3p, miR-20b-5p, miR-345-3p, and the miR-15 cluster have been associated with immune or stress responses (58– 62). [score:2]
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Initially we conducted genome-wide transcriptional profiling of miRNAs and mRNAs, as depicted in Figures 1– 4. When thymocytes where compared to naïve T cells, we noticed that some miRNAs, including miR-30e, miR-363 and miR-130b, did not show altered expression. [score:2]
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[+] score: 2
Other miRNAs from this paper: hsa-mir-130b
P53 mutations in the DBD were shown to increase metastasis through induction of EMT via several routes including sequestration of p63, stabilization/activation of SLUG/SNAIL, induction of the mir130b-Zeb1 axis, TWIST and SLUG transcription factors and other mechanisms [12, 38– 42]. [score:2]
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Since miRNAs can have different aliases, the 10 miRNAs (Fig 1) are identified as the following for the rest of this manuscript: let-7 = let-7b, let-7a-5p = let-7c, miR-10 = miR-10b, miR-130 = miR-130a, miR-155 = miR-155, miR-27 = miR27a, miR-24-3p = miR-24, miR-17 = miR-18a, miR-15 = miR-15a, and miR-16-5p = miR-497. [score:1]
This miRNA signature consists of 10 miRNAs: miR-130, miR-27, miR-17, miR-10, miR-155, let-7a-5p, let-7, miR-24-3p, miR-15, and miR-16-5p. [score:1]
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As shown in Figure 5D, miRNAs miR-19a, miR-21, miR-27a, miR-130 and miR-146a were enriched within exosomes and virtually undetectable as free, circulating miRNAs in the supernatant. [score:1]
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P <0.01 for miR-17, 18a, 19b-1, 20a, 92a-1 and 210, P < 0.05 for miR-19a, 126 and 296 and P > 0.05 for miR-130. [score:1]
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The sub-network I is composed of three clusters including miR-17-92, miR-106b-25 and miR-15b-16 clusters, and two paralogous miRNAs miR-103 and miR-107 as well as three unrelated miRNAs including let-7i, miR-130b and miR-140-5p. [score:1]
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To address these limitations, we developed a predictive algorithm that differentiates early-stage cancers from benign tumors using 7 miRNAs (miR-200a-3p, miR-766-3p, miR-26a-5p, miR-142-3p, let-7d-5p, miR-130b-3p and miR-328-3p). [score:1]
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These miRNAs include miR-29a/b, miR-100, miR-107, miR-130b, miR-193b, miR-343-3p, miR-351, and miR-455. [score:1]
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Here, 15 miRNAs (miR-let-7e*, miR-15a*, miR-19b-1*, miR-30e*, miR-130b*, miR-149, miR-296-5p, miR-362-5p, miR-378, miR-425, miR-432, miR-484, miR-574-3p, miR-671-5p, and miR-1249) established interactions with 19 mRNAs. [score:1]
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H poly mmu-miR-150 mmu-miR-181a ↓↓ ↓↓ mmu-miR-669f ↓ ↓ mmu-miR-29c ↑ mmu-miR-155 ↑ ↑ mmu-miR-467f mmu-miR-466a/b-3p ↓ ↓ mmu-miR-361 ↑↑ ↓ mmu-miR-547 mmu-miR-1949 mmu-miR-345-3p ↓ ↑ mmu-miR-101b mmu-miR-340-5p mmu-miR-148a ↑ ↑ mmu-miR-139-5p ↓↓ ↓ mmu-miR-132 ↑ ↑ mmu-miR-539 ↓ mmu-miR-125a-5p ↑↑ ↑ ↓ mmu-miR-130b *miRNAs with Nanostring counts that passed the minimum intensity filter and have >2-fold differences among any two-way comparison. [score:1]
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Four of these p63-miRNA feedback-related pairs (ΔNp63/miR-130b, ΔNp63/miR-92, ΔNp63/miR-181a-5p and ΔNp63/miR-374a-5p) have been validated [24– 27]. [score:1]
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These data suggested that miR-130 might act to antagonize curcumin’s anti-tumor effect. [score:1]
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Log FC offset P-val (a) P-val (b) hsa-mir-19a Early 125/50.20% −2.485 0.031 1.5023E-05 2.19E-06 hsa-mir-106 Early 156/56.52% −3.929 0.030 2.3594E-05 3.10E-07 hsa-mir-181a Early 125/49.02% −0.242 0.029 0.0001 3.42E-06 miR-93 Early 72/50.35% −3.272 0.030 0.0019 1.78E-05 mmu-mir-153 Early 75/48.08% −0.610 0.036 0.0108 0.0088 hsa-mir-92-1,2 Early 128/55.65% −5.035 0.024 0.0109 0.0001 miR-130 Early 99/57.56% −1. [score:1]
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Other miRNAs from this paper: hsa-mir-25, hsa-mir-28, hsa-mir-95, mmu-mir-151, mmu-mir-290a, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-340, mmu-mir-25, mmu-mir-28a, hsa-mir-130b, hsa-mir-367, hsa-mir-372, hsa-mir-378a, mmu-mir-378a, hsa-mir-340, hsa-mir-151a, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-505, hsa-mir-506, mmu-mir-367, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-648, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-659, hsa-mir-421, hsa-mir-151b, hsa-mir-1271, hsa-mir-378d-2, mmu-mir-467b, mmu-mir-297b, mmu-mir-505, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-421, 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-467c, mmu-mir-467d, mmu-mir-92b, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-669g, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, mmu-mir-1195, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1289-1, hsa-mir-1289-2, hsa-mir-548k, hsa-mir-1299, hsa-mir-548l, hsa-mir-1302-1, hsa-mir-1302-2, hsa-mir-1302-3, hsa-mir-1302-4, hsa-mir-1302-5, hsa-mir-1302-6, hsa-mir-1302-7, hsa-mir-1302-8, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1255a, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-1268a, 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-1255b-1, hsa-mir-1255b-2, mmu-mir-1906-1, hsa-mir-1972-1, hsa-mir-548q, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-3116-1, hsa-mir-3116-2, hsa-mir-3118-1, hsa-mir-3118-2, hsa-mir-3118-3, hsa-mir-548s, hsa-mir-378b, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3156-1, hsa-mir-3118-4, hsa-mir-3174, hsa-mir-3179-1, hsa-mir-3179-2, hsa-mir-3179-3, hsa-mir-548w, hsa-mir-3156-2, hsa-mir-3156-3, hsa-mir-548x, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-3471-1, mmu-mir-3471-2, hsa-mir-378c, hsa-mir-1972-2, hsa-mir-1302-9, hsa-mir-1302-10, hsa-mir-1302-11, mmu-mir-1906-2, hsa-mir-3683, hsa-mir-3690-1, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, mmu-mir-28c, mmu-mir-378b, mmu-mir-28b, hsa-mir-548ao, hsa-mir-548ap, mmu-mir-466q, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, mmu-mir-378c, mmu-mir-378d, hsa-mir-548ay, hsa-mir-548az, hsa-mir-3690-2, mmu-mir-290b, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-3179-4, mmu-mir-466c-3, hsa-mir-548bc, mmu-mir-1271
Exceptions to this were hsa-mir-130b and hsa-mir-648 that we classified as NRdmiRs, and hsa-mir-659 that was classified as a PRdmiR. [score:1]
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