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PFN2a Suppresses C2C12 Myogenic Development by Inhibiting Proliferation and Promoting Apoptosis via the p53 Pathway

文献类型： 外文期刊

作者： Li, Huaqin 1 ; Hou, Lianjie 1 ; Zhang, Yu 1 ; Jiang, Fangyi 1 ; Zhu, Yifan 1 ; Li, Qing X. 2 ; Hu, Ching Yuan 3 ; Wang, C 1 ;

作者机构： 1.South China Agr Univ, Coll Anim Sci, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Natl Engn Res Ctr Breeding Swine Ind, Guangzhou 510642, Guangdong, Peoples R China

2.Univ Hawaii Manoa, Dept Mol Biosci & Bioengn, 1955 East West Rd, Honolulu, HI 96822 USA

3.Univ Hawaii Manoa, Dept Human Nutr Food & Anim Sci, 1955 East West Rd, Honolulu, HI 96822 USA

关键词： proliferation; myogenic development; skeletal muscle; apoptosis; HDAC1

期刊名称：CELLS （ 影响因子：6.6； 五年影响因子：6.663 ）

ISSN：

年卷期： 2019 年 8 卷 9 期

页码：

收录情况： SCI

摘要： Skeletal muscle plays a crucial role in physical activity and in regulating body energy and protein balance. Myoblast proliferation, differentiation, and apoptosis are indispensable processes for myoblast myogenesis. Profilin 2a (PFN2a) is a ubiquitous actin monomer-binding protein and promotes lung cancer growth and metastasis through suppressing the nuclear localization of histone deacetylase 1 (HDAC1). However, how PFN2a regulates myoblast myogenic development is still not clear. We constructed a C2C12 mouse myoblast cell line overexpressing PFN2a. The CRISPR/Cas9 system was used to study the function of PFN2a in C2C12 myogenic development. We find that PFN2a suppresses proliferation and promotes apoptosis and consequentially downregulates C2C12 myogenic development. The suppression of PFN2a also decreases the amount of HDAC1 in the nucleus and increases the protein level of p53 during C2C12 myogenic development. Therefore, we propose that PFN2a suppresses C2C12 myogenic development via the p53 pathway. Si-p53 (siRNA-p53) reverses the PFN2a inhibitory effect on C2C12 proliferation and the PFN2a promotion effect on C2C12 apoptosis, and then attenuates the suppression of PFN2a on myogenic differentiation. Our results expand understanding of PFN2a regulatory mechanisms in myogenic development and suggest potential therapeutic targets for muscle atrophy-related diseases.

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