miR‐483 inhibits bovine myoblast cell proliferation and differentiation via <i>IGF1/PI3K/AKT</i> signal pathway

Song, Chengchuang; Dong, Dong; Xu, Jie; Wang, Jian; Li, Hui; Huang, Yongzhen; Lan, Xianyong; Lei, Chuzhao; Ma, Yun; Chen, Hong

doi:10.1002/jcp.27672

Cited by 36 publications

(35 citation statements)

References 42 publications

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“…Interestingly, in this study, miR-146a-5p repressed both proliferation and differentiation of intramuscular preadipocytes. Literatures indicated that miR-483 inhibited both the proliferation and differentiation of bovine myoblasts [32], as well as miR-342-5p restricted the proliferation and differentiation of osteoblasts by inhibiting the expression of Bmp7 [33]. Therefore, our results were reasonable because of complexity of the biological processes of intramuscular preadipocytes via miRNA regulation.…”

Section: Discussionsupporting

confidence: 60%

MiR-146a-5p Targeting SMAD4 and TRAF6 Inhibits Adipogenensis Through TGF-β and NF-κB Signal Pathways in Porcine Intramuscular Preadipocytes

Zhang

Cai

Tang

et al. 2020

Preprint

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Background: Intramuscular fat (IMF) content is a vital parameter to assess pork quality. Increasing evidences have shown that microRNAs (miRNAs) play an important role in regulating porcine IMF deposition. Here, a novel miRNA implicated in porcine IMF adipogenesis was found, and its effect and regulatory mechanism was further explored on the proliferation and differentiation of intramuscular preadipocytes.Results: By miRNAs sequencing analysis in porcine adipose tissues, we found that miR-146a-5p was a potential regulator of porcine IMF adipogenesis. Further study showed that miR-146a-5p mimics inhibited the proliferation of porcine intramuscular preadipocytes, but its inhibitor promoted cell proliferation. Interestingly, miR-146a-5p mimics also repressed preadipocyte differentiation, whereas its inhibitor promoted adipogenic differentiation. Mechanistically, miR-146a-5p suppressed cell proliferation by directly targeting SMAD family member 4 (SMAD4) to attenuate the TGF-β signal. Moreover, miR-146a-5p inhibited the differentiation of intramuscular preadipocytes by targeting TNF receptor associated factor 6 (TRAF6) to weaken the NF-κB signaling of the TRAF6 downstream pathway.Conclusions: MiR-146a-5p targeting SMAD4 and TRAF6 inhibited porcine intramuscular adipogenesis through attenuating TGF-β and NF-κB signals, respectively. These findings provided a novel miRNA biomarker for regulating intramuscular adipogenesis to promote pork quality.

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Section: Discussionsupporting

confidence: 60%

MiR-146a-5p Targeting SMAD4 and TRAF6 Inhibits Adipogenensis Through TGF-β and NF-κB Signal Pathways in Porcine Intramuscular Preadipocytes

Zhang

Cai

Tang

et al. 2020

Preprint

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“…As shown in Figure A, miR‐1914 overexpression dramatically decreased p‐AKT and mTOR levels, whereas miR‐1914 silencing increased p‐AKT and mTOR levels in HCC cells. As previously reported, IGF‐1, an AKT activator, plays a vital role in the activation of the PI3K/AKT pathway. To determine whether AKT phosphorylation mediated the effects of miR‐1914, an inhibitor (MK2206) and activator (IGF‐1) of AKT were applied to modulate the status of AKT phosphorylation.…”

Section: Resultsmentioning

confidence: 58%

microRNA‐1914, which is regulated by lncRNA DUXAP10, inhibits cell proliferation by targeting the GPR39‐mediated PI3K/AKT/mTOR pathway in HCC

Sun

Wang

Chen

et al. 2019

J Cellular Molecular Medi

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Increasing studies have confirmed that abnormally expressed microRNAs (miRNAs) take part in the carcinogenesis as well as the aggravation of hepatocellular carcinoma (HCC). However, little information is currently available about miR‐1914 in HCC. Here, we first confirmed that miR‐1914 inhibition in HCC cell lines and tumour specimens correlates with tumour size and histological grade. In a series of functional experiments, miR‐1914 inhibited tumour proliferation and colony formation, resulting in cell cycle arrest and increased apoptosis. Moreover, miR‐1914 mediated its functional effects by directly targeting GPR39 in HCC cells, leading to PI3K/AKT/mTOR repression. Restoring GPR39 expression incompletely counteracted the physiological roles of miR‐1914 in HCC cells. In addition, down‐regulation of AKT phosphorylation inhibited the effects of miR‐1914 in HCC. Furthermore, the overexpression of lncRNA DUXAP10 negatively correlated with the expression of miR‐1914 in HCC; thus, lncRNA DUXAP10 regulated miR‐1914 expression and modulated the GPR39/PI3K/AKT‐mediated cellular behaviours. In summary, the present study demonstrated for the first time that lncRNA DUXAP10–regulated miR‐1914 plays a functional role in inhibiting HCC progression by targeting GPR39‐mediated PI3K/AKT/mTOR pathway, and this miRNA represents a novel therapeutic target for patients with HCC.

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“…Recent research have investigated the functional mechanism of miRNAs in influencing bovine skeletal muscle cell proliferation and differentiation (Dai et al, 2016;Song et al, 2018;Tong, Jiang, Zhang, & Yan, 2017;, but merely a few miRNAs in regulation of muscle cells apoptosis (Wei et al, 2017). In present study, we investigated the expression characteristic of miR-148a-3p…”

Section: Discussionmentioning

confidence: 99%

miR‐148a‐3p regulates proliferation and apoptosis of bovine muscle cells by targeting KLF6

Yang

Jiang

Song

et al. 2019

Journal Cellular Physiology

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Skeletal muscle development is regulated by a series of regulatory factors, and also including noncoding RNA, especially microRNAs (miRNAs). Recently, miR‐148a has been found to be involved in murine C2C12 differentiation by targeting ROCK1. However, the function of miR‐148a‐3p for the proliferation and apoptosis of bovine muscle cells has not been determined. In this study, we found that miR‐148a‐3p was highly expressed in fetal bovine skeletal muscle and exhibited a decreasing trend in muscle cells during its growth phase. Functional studies indicated that gain of miR‐148a‐3p inhibited the proliferation of bovine muscle cells and promoted apoptosis. Conversely, interference with miR‐148a‐3p inhibitor promoted muscle cell proliferation and inhibited its apoptosis. Mechanistically, KLF6 was confirmed as a new potential target gene of miR‐148a‐3p by TargetScan software prediction and the dual‐luciferase assay verification. Additionally, after a gain or loss of KLF6, the function of KLF6 for muscle cell proliferation and apoptosis was opposite to that of miR‐148a‐3p. Collectively, these findings proposed a novel avenue whereby miR‐148a‐3p impeded bovine myoblast cell proliferation and promoted apoptosis through the posttranscriptional downregulation of KLF6.

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miR‐483 inhibits bovine myoblast cell proliferation and differentiation via IGF1/PI3K/AKT signal pathway

Cited by 36 publications

References 42 publications

MiR-146a-5p Targeting SMAD4 and TRAF6 Inhibits Adipogenensis Through TGF-β and NF-κB Signal Pathways in Porcine Intramuscular Preadipocytes

MiR-146a-5p Targeting SMAD4 and TRAF6 Inhibits Adipogenensis Through TGF-β and NF-κB Signal Pathways in Porcine Intramuscular Preadipocytes

microRNA‐1914, which is regulated by lncRNA DUXAP10, inhibits cell proliferation by targeting the GPR39‐mediated PI3K/AKT/mTOR pathway in HCC

miR‐148a‐3p regulates proliferation and apoptosis of bovine muscle cells by targeting KLF6

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