Abstract: Objective To identify whether cisplatin can induce autophagy of bladder cancer T24 cells and the possible mechanism, and observe the relationship between outophagy and apoptosis. Methods MTT assay was applied to investigate the effects of various concentration of cisplatin(0, 10, 20 and 40 μg/mL) on T24 survival. TEM detection of autophagosome formation. Western blotting assay was used to analyze the expression changes of LC3-II, P62 and extracellular signal-regulated kinase (ERK1/2) and p-ERK at the protein level. The effects of autophagy on the survival and apoptosis of bladder cancer cells were investigated. Results DDP could observably inhibite proliferation of bladder cancer cells in a dose-dependent manner （P < 0.05）， the 50% inhibiting concentration(IC50) was （30.3±2.4）μg/mL; DDP could induce autophagy of bladder cancer cells, observably increased autophagosome induced by DDP; up-regulated expression levels of LC3-II proteins （P < 0.05）, down-regulated expression levels of P62 proteins （P < 0.05）; DDP could increase the protein level of p-ERK （P < 0.05）; The inhibitor of ERK pathway U0126 inhibited DDP-induced autophagy, as evidenced by decrease in the expression of LC3-II proteins （P < 0.05）. After the inhibition of autophagy by WTM in DDP-treated cells, cell viability was obviously decreased and apoptosis was increased （P < 0.05）; DDP combined with WTM observably enhanced cleavage of poly ADP-ribose polymerase 1 (PARP-1) and cleaved-caspase3 which are apoptosis related proteins（P < 0.05）. Conclusion Autophagy can protect T24 cells against ciplatin-induced apoptosis, the possible mechanism of autophagy is the ERK signaling pathway activation.

Key words: bladder cancer, cisplatin, autophagy, p-ERK