| Objective To investigate the mechanism by which epirubicin(EPI)induces autophagy and the mechanism by which tea polyphenol(TP)regulates EPI-induced autophagy and apoptosis in T24 bladder cancer cell line.Methods Cells were divided into control group,EPI group,TP group and TP plus EPI group for indicated time.Transmission electron microscope(TEM)was used to observe the image of autophagosomes.Apoptotic cells were evaluated by flow cytometry.Western blot was applied to detect the level of LC3-II,p62,CASP3 and PARP.Results Compared with control group,cell viability in TP plus EPI group is much lower than that in EPI group(P<0.05).The amount of autophagosomes and the level of LC3-II in TP plus EPI group were much higher than those in EPI group.SP,an inhibitor of JNK pathway,reduced the level of LC3-II induced by EPI.EPI activated p-JNK in a time-dependent manner.Compared with control group,the apoptosis rate and the level of activated apoptotic protein in TP plus EPI group were much higher than those in EPI group.Conclusion TP inhibits JNK-mediated autophagy to sensitize EPI-induced apoptosis in human bladder cancer cells. |