姜黄素通过抑制乙酰转移酶P300表达促进HeLa细胞凋亡OA北大核心CSTPCD

AIM:To investigate the effect of curcumin on the viability and apoptosis of human papillomavirus(HPV)-positive cervical cancer cells via down-regulating the expression of adenovirus E1A-associated 300 kD protein(P300).METHODS:HeLa cells in logarithmic phase were divided into four experimental groups(20,40,60 and 80 µmol/L Cur treatment groups),and the untreated group was used as control.Cell apoptosis was detected by flow cytome-try,and the expression of E6 gene was detected by RT-qPCR and Western blot.Silencing plasmid(shE6)and negative control shRNA(shNC)were constructed and transfected into HeLa cells,the cells were randomly divided into four groups including shNC,shNC+Cur(40 µmol/L),shE6 and shE6+Cur(40 µmol/L).The cell viability,apoptosis and expression of apoptosis-related proteins were detected by CCK-8,flow cytometry and Western blot,respectively.Then silencing plas-mid(siP300)and negative control siRNA(siNC)were constructed and transfected into HeLa cells.The mRNA and pro-tein expression of P300 was detected by RT-qPCR and Western blot.The protein expression of E6 and P300 and histone was detected by Western blot after treated with 20 and 40 µmol/L curcumin.RESULTS:Compared with the untreated group,the HeLa cells treated with different concentrations of curcumin could significantly inhibit the viability and increase the early apoptosis rate(P<0.05).The results showed that the mRNA and protein expression of E6 were down-regulated in HeLa cells after treated with different concentration curcumin,while the early apoptosis and the expression of pro-apop-tosis-related proteins in the shE6 group were lower than those in the non-knockdown group after treated with 40 µmol/L cur-cumin(P<0.05).And the expression of E6 protein was decreased after knockdown of P300,while the expression of P300 and histone was down-regulated after treatment with 20 and 40 µmol/L curcumin.CONCLUSION:Curcumin can inhibit the viability and promote the apoptosis of HPV18 positive cervical cancer cells,and the mechanism may be that it can in-hibit E6 acetylation by down-regulating P300 expression.