Effect Of Curcumol On Proliferation And Apoptosis And EZH2 Expression In Bladder Cancer Cells

Objective: Our previous study showed that EZH2 was highly expressed in bladder cancer and played an important role in the development of bladder cancer.Moreover,it’s reported that curcumol could affect the growth and survival of multiple kinds of tumors.Therefore,this study aims to investigate the effect of curcumol on the growth and EZH2 expression in human bladder cancer cell lines EJ and T24,and discuss the possible mechanism.Methods: The bladder cancer EJ and T24 cells were cultured in vitro,and incubated with different concentrations of curcumol(0,12.5,25,50,100mg/L).CCK-8 assay and the colony formation test were adopted to evaluate the inhibitory effect of curcumol on the proliferation of cancer cells.Flow cytometry technique was used to detect the apoptosis effect of curcumol on each experimental group.The expression of EZH2 mRNA was examined with Quantitative Real-Time polymerase chain reaction(qRT-PCR),and the expression of EZH2 protein was detected by Western Blot.Results: CCK-8 assay showed that with the increase of drug concentration and the prolongation of incubation time,the inhibitory effect of curcumol on the proliferation of EJ and T24 cells increased significantly.The colony formation test also indicated that compared with control,curcumol could significantly inhibit the growth of EJ and T24 cells.The apoptosis rate of EJ cells was(0.50±0.05)%,(3.60±0.60)%,(6.20±1.00)%,(16.50±1.50)% and(29.00±2.15)%,the difference was statistically significant.The apoptosis rate of T24 cells was(2.40±0.10)%,(4.93±0.15)%,(6.03±0.15)%,(13.50±0.89)% and(25.80±0.66)%,the difference was statistically significant.Apoptosis induced by curcumol in EJ and T24 cells was in a concentration dependent manner.Both qRT-PCR and Western Blot results showed that curcumol can significantly inhibit EZH2 gene expression.Conclusions: Curcumol could significantly inhibit the proliferation and induce the apoptosis of EJ and T24 cells,which may be related to the down-regulation of EZH2.