5-Aza-2'-deoxycytidine may influence the proliferation and apoptosis of cervical cancer cells via demethylation in a dose- and time-dependent manner.
Genet Mol Res
; 12(1): 312-8, 2013 Feb 04.
Article
em En
| MEDLINE
| ID: mdl-23408418
ABSTRACT
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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Azacitidina
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Neoplasias do Colo do Útero
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Apoptose
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Metilação de DNA
Limite:
Female
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Humans
Idioma:
En
Ano de publicação:
2013
Tipo de documento:
Article