TWIST1 promotes cell viability and migration, but inhibits apoptosis in MC3T3 cells via regulating PI3K and p16 pathways

Background: Osteoporosis, a disease of the skeleton, results in an increased risk of fracture. Its characters are the loss of bone mass and degeneration of bone microstructure. This study was aimed to demonstrate an essential function of Twist-related protein 1 (TWIST1)-on osteoporosis. Methods: The expression of TWIST1 was overexpressed or silenced by specific transfection in MC3T3 cells and then were confirmed by real-time polymerase chain reaction (RT-PCR) and Western blot. The cell viability and cell migration were determined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and Transwell cell migration assay, respectively. Furthermore, cell apoptosis was analyzed by flow cytometry, and the protein expression of phosphatidyl inositide 3-kinases (PI3K) or p16 pathways related proteins was measured. Results: Here, this study showed that MC3T3 cells viability and migration were significantly increased by TWIST1 overexpression compared to the control group (P < 0.05), but the cell apoptosis was statistically decreased (P < 0.05). However, while TWIST1 silencing, the cells viability and migration were significantly appeared to be decreased, accompanied by apoptosis increasing (P < 0.05). Furthermore, the protein expression of PI3K and protein kinase B (p-Akt) were significantly increased (P < 0.05), but p16 and phosphorylate retinoblastoma protein (p-RB) were significantly decreased (P < 0.05). Conclusions: These results highlight the importance of TWIST1 to the target of treating osteoporosis. TWIST1 could promote cell viability and migration, but inhibit apoptosis in MC3T3 cells via regulating PI3K and p16 pathways.