| Summary: | 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 <i>PFN2a</i> regulates myoblast myogenic development is still not clear. We constructed a C2C12 mouse myoblast cell line overexpressing <i>PFN2a</i>. The CRISPR/Cas9 system was used to study the function of <i>PFN2a</i> in C2C12 myogenic development. We find that <i>PFN2a</i> suppresses proliferation and promotes apoptosis and consequentially downregulates C2C12 myogenic development. The suppression of <i>PFN2a</i> also decreases the amount of HDAC1 in the nucleus and increases the protein level of p53 during C2C12 myogenic development. Therefore, we propose that <i>PFN2a</i> suppresses C2C12 myogenic development via the p53 pathway. Si-<i>p53</i> (siRNA-<i>p53</i>) reverses the <i>PFN2a</i> inhibitory effect on C2C12 proliferation and the <i>PFN2a</i> promotion effect on C2C12 apoptosis, and then attenuates the suppression of <i>PFN2a</i> on myogenic differentiation. Our results expand understanding of <i>PFN2a</i> regulatory mechanisms in myogenic development and suggest potential therapeutic targets for muscle atrophy-related diseases.
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