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The  methylation of tumor suppressor genes has been shown to be involved in many  human cancers. 5-Aza-2'-deoxycytidine  (5-Aza-CdR) can reactivate the expression of methylated tumor suppressor genes.  In our study, 2 human cervical cancer cell lines, HeLa and SiHa, were treated  with different concentrations (20, 10, 5, and 2.5 μM) of 5-Aza-CdR for 24, 48, and 72  h. After incubation, cells were analyzed by  3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay and flow  cytometry. The expression of RASSF1A and APAF-1 was detected by  RT-PCR. 5-Aza-CdR inhibited the growth of HeLa and SiHa cells at different  concentrations. The strongest inhibition and apoptosis rates were obtained  after incubation for 72 h (5.63 ± 1.38 and 8.24 ± 2.40%, respectively). No  significant difference in the expression of RASSF1A was found upon drug  treatment, while APAF-1 expression increased in HeLa cells after  treatment (0.790 ± 0.056%). Our results suggest that the tumor-suppressive  effect of 5-Aza-CdR may result from the reactivation of silenced APAF-1 through  demethylation.

5-Aza-2’-deoxycytidine may influence the proliferation and apoptosis of cervical cancer cells via demethylation in a dose- and time-dependent manner