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

被引:43
|
作者
Song, Chengchuang [1 ]
Yang, Jiameng [1 ]
Jiang, Rui [1 ]
Yang, Zhaoxin [1 ]
Li, Hui [1 ]
Huang, Yongzhen [1 ]
Lan, Xianyong [1 ]
Lei, Chuzhao [1 ]
Ma, Yun [2 ]
Qi, Xinglei [3 ]
Chen, Hong [1 ]
机构
[1] Northwest A&F Univ, Coll Anim Sci & Technol, Key Lab Anim Genet Breeding & Reprod Shaanxi Prov, Yangling, Shaanxi, Peoples R China
[2] Xinyang Normal Univ, Inst Conservat & Utilizat Agrobioresources Dabie, Coll Life Sci, Xinyang, Henan, Peoples R China
[3] Bur Anim Husb Biyang Cty, Biyang, Henan, Peoples R China
基金
中国国家自然科学基金;
关键词
apoptosis; KLF6; miR-148a-3p; proliferation; SKELETAL-MUSCLE; MYOGENIC DIFFERENTIATION; MYOBLAST PROLIFERATION; PROMOTES APOPTOSIS; EXPRESSION; MICRORNAS; BCL-2;
D O I
10.1002/jcp.28232
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:15742 / 15750
页数:9
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