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

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 regulates myoblast myogenic development is still not clear. We constructed a C2C12 mouse myoblast cell line overexpressing . The CRISPR/Cas9 system was used to study the function of in C2C12 myogenic development. We find that suppresses proliferation and promotes apoptosis and consequentially downregulates C2C12 myogenic development. The suppression of also decreases the amount of HDAC1 in the nucleus and increases the protein level of p53 during C2C12 myogenic development. Therefore, we propose that suppresses C2C12 myogenic development via the p53 pathway. Si- (siRNA-) reverses the inhibitory effect on C2C12 proliferation and the promotion effect on C2C12 apoptosis, and then attenuates the suppression of on myogenic differentiation. Our results expand understanding of regulatory mechanisms in myogenic development and suggest potential therapeutic targets for muscle atrophy-related diseases.