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Proliferation of bovine myoblast by LncPRRX1 via regulation of the miR-137/CDC42 axis
International Journal of Biological Macromolecules ( IF 7.7 ) Pub Date : 2022-08-06 , DOI: 10.1016/j.ijbiomac.2022.08.018
Wenzhen Zhang 1 , Bing Sun 1 , Yanqing Zhao 1 , Sayed Haidar Abbas Raza 1 , Yishu Li 2 , Jianfang Wang 1 , Xinhao Ma 1 , Hailah M Almohaimeed 3 , Sameerah Shaheen 4 , Faisal Al-Sarraj 5 , Raed Albiheyri 6 , Chugang Mei 1 , Linsen Zan 7
Affiliation  

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.



中文翻译:

LncPRRX1通过调节miR-137/CDC42轴增殖牛成肌细胞

非编码 RNA,如长链非编码 RNA (lncRNA),在牲畜中含量丰富。许多影响牲畜生长速度的 lncRNA 已在肌肉中发现。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,我们鉴定了一种新的 lncRNA (lncPRRX1) 并研究了它对牛成肌细胞增殖的影响。LncPRRX1在肌肉组织中高表达,干扰lncPRRX1可抑制体外牛成肌细胞的增殖。lncPRRX1 的 RNA 分子作为竞争性内源性 RNA (ceRNA) 作用于 miR-137。miR-137的过表达抑制了成肌细胞的增殖,而miR-137的抑制则具有相反的效果。此外,miR-137的预测靶基因在丝裂原活化蛋白激酶(MAPK)信号通路中显着富集,其中细胞分裂周期42(CDC42)被证明是miR-137的直接靶基因,并干扰CDC42抑制成肌细胞增殖。此外,干扰lncPRRX1修复了由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轴促进牛成肌细胞增殖。

更新日期:2022-08-06
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