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LncPRRX1 通过调控 miR-137/CDC42 轴促进牛肌卫星细胞的增殖。

Proliferation of bovine myoblast by LncPRRX1 via regulation of the miR-137/CDC42 axis.

机构信息

College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, PR China.

College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, PR China.

出版信息

Int J Biol Macromol. 2022 Nov 1;220:33-42. doi: 10.1016/j.ijbiomac.2022.08.018. Epub 2022 Aug 6.

DOI:10.1016/j.ijbiomac.2022.08.018
PMID:35944756
Abstract

Noncoding RNAs, such as long noncoding RNAs (lncRNAs), are abundant in livestock. Many lncRNAs that affect the growth rate of livestock have been identified in muscles. However, some of their physiological functions and regulatory mechanisms remain unclear. In this study, we identified a new lncRNA (lncPRRX1) and investigated its effect on the proliferation of bovine myoblasts. LncPRRX1 was highly expressed in muscle tissue, and interference with lncPRRX1 inhibited the proliferation of bovine myoblasts in vitro. The RNA molecules of lncPRRX1 act on miR-137 as competitive endogenous RNAs (ceRNAs). Overexpression of miR-137 suppressed the proliferation of myoblasts, while inhibition of miR-137 had the opposite effect. In addition, the predicted target genes of miR-137 were significantly enriched in the mitogen-activated protein kinase (MAPK) signaling pathway, in which Cell Division Cycle 42 (CDC42) was shown to be the direct target gene of miR-137, and interference with CDC42 inhibited myoblast proliferation. Furthermore, interference with lncPRRX1 repaired the defects in CDC42 protein levels and cell proliferation caused by miR-137 inhibitors. Our results suggested that lncPRRX1 promoted bovine myoblast proliferation by regulating the miRNA-137/CDC42 axis.

摘要

非编码 RNA ,如长非编码 RNA (lncRNA) ,在牲畜中大量存在。在肌肉中已经鉴定出许多影响牲畜生长速度的 lncRNA 。然而,它们的一些生理功能和调节机制仍不清楚。在这项研究中,我们鉴定了一个新的 lncRNA (lncPRRX1) ,并研究了它对牛肌细胞增殖的影响。lncPRRX1 在肌肉组织中高度表达,干扰 lncPRRX1 抑制牛肌细胞在体外的增殖。lncPRRX1 的 RNA 分子作为竞争性内源性 RNA (ceRNA) 作用于 miR-137 。miR-137 的过表达抑制肌细胞的增殖,而抑制 miR-137 则有相反的效果。此外,miR-137 的预测靶基因在丝裂原活化蛋白激酶 (MAPK) 信号通路中显著富集,其中细胞分裂周期蛋白 42 (CDC42) 被证明是 miR-137 的直接靶基因,干扰 CDC42 抑制肌细胞增殖。此外,干扰 lncPRRX1 修复了 miR-137 抑制剂引起的 CDC42 蛋白水平和细胞增殖缺陷。我们的结果表明,lncPRRX1 通过调节 miRNA-137/CDC42 轴促进牛肌细胞增殖。

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