Cell cycle arrest and autophagy induced by celecoxib in human HepG2 cells
Objective To investigate the effect of celecoxib on the cell cycle and cell autophagy of HepG2 cell line and its possible molecular mechanism. Methods HepG2 cells were treated with celecoxib at different concentrations (0, 50, 100, 200, 500μM), then MTT was used to detect the cell proliferation, cell cycle and apoptosis were detected by flow cytometry, the cell autophagy was observed by transmission electron microscopy, and the expressions of cyclin and autophagy protein were determined using Western blot. Results Celecoxib inhibited the proliferation of HepG2 cells in a concentration dependent manner (0, 50, 100, 200 and 500 μM) and time-dependent manner (24,48h)(P<0.05). There was no significant change in necrocytosis and apoptosis after ttreated by different concentrations of (0, 50, 100, 200 and 500 μM). The celecoxib inhibited cell cycle arrest at G1 phase, the cell rate of G1 phase increased, while the cell rate of S phase decreased in a concentration dependent manner (0, 50, 100, 200 and 500 μM) and time-dependent manner (0, 8, 16, 24h)(P<0.05). The protein expressions of cyclin D1,cyclin D3, cyclin E2, CDK2 and CDK4 significantly decreased by 500 μM celecoxib (P<0.05). The celecoxib induced autophagy in HepG2 cells, and transformed autophagy protein LC3-Ⅰto LC3-Ⅱ in a concentration dependent manner. Conclusion Celecoxib can effectively inhibit the proliferation of human malignant hepatocellular carcinoma cell line HepG2, which provides a new idea for the clinical application of celecoxib.
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