Mechanical stress promotes biological functions of C2C12 myoblasts by activating PI3K/AKT/mTOR signaling pathway

The PI3K/AKT signaling pathway regulates cell proliferation and differentiation in multiple types of cells. The present study aimed to investigate the effects of mechanical stress on C2C12 cell proliferation and to explore the associated mechanisms. A cyclic mechanical stress model of C2C12 myoblasts was established. Reverse transcription-quantitative PCR and western blotting assay were used to examine the PI3K signaling pathways involved in the progress of cell differentiation. Cell counting kit-8 (CCK-8) assay was used to evaluate the proliferation of C2C12 cells. Flow cytometry was employed to evaluate apoptosis following mechanical stress. The results demonstrated that mechanical stress activated the PI3K signaling pathway in C2C12 myoblasts. Mechanical stress significantly promoted phosphorylation (p-) of AKT and expression of mammalian target of rapamycin (mTOR) compared with the normal group. Mechanical stress significantly promoted 4E-binding protein 1 (4EBP1) expression in C2C12 cells compared with the normal group. The PI3K specific inhibitor LY294002 significantly decreased 4EBP1 expression and reduced p-AKT and p-mTOR expression compared with the mechanical stress group. Mechanical stress promoted C2C12 cell proliferation. Apoptosis of C2C12 significantly decreased in the mechanical stress group compared with the normal group. Cyclin D levels significantly increased in the mechanical stress group compared with the normal group. In conclusion, mechanical stress promoted biological functions of C2C12 cells by activating the PI3K/AKT signaling pathway. These results may contribute to a better understanding of the effects of mechanical stress on cells.