Methylation In Estrogen And Progesterone Receptor Of Endometrial Carcinoma Cells Contributes To Receptors Expression And Cells Growth

ObjectiveTo detect the methylation status in the promoter region of the ER,PR genein endometrial carcinoma and the impact on ER,PR gene expression withdemethylation medicine. The relationship between the decrease of ER,PR geneexpression and the gene aberrant methylation, and the influence on endometrialcarcinoma cells antigrowth and inducing apoptosis by reverses ER,PR genehypermethylation was investigated.MethodsThe methylation status of ER,PR isoforms were analyzed bymethylation-specific-PCR method and western blot analysis respectively,endometrial carcinoma cell lines(HEC-1-B, Ishikawa)treated with and treatedwithout ADC. The effect of different ADC and MA concentration on cellantigrowth was assayed by MTT methods, inducing the cell apoptosis wasmeasured by acridine orange-ethidium bromide (AO-EB) double fluorescent dyestaining.ResultsIn the Hec-1-B,Ishikawa cell lines only ERα-c,PRB were methylated.Treated with ADC the expression of ERα and PRB proteins were enhanced. Recover the ability of MA to inhibit and inducing apoptosis the Hec-1-B cells withthe ADC, the endometrial carcinoma cells showed a dramatic antigrowth andcell apoptosis rate increases with the MA concentration.ConclusionsThere is a hypermethylation in ERα-c and PRB gene promoterregions,maybe the reason for the expression of ERα and PRB proteindescended or deficiency.ADC not only change the gene hypermethylation status,but also could reverse the protein expression. Meanwhile recover the ER,PRgene expression with ADC,MA could better inhibit the endometrial carcinomacells proliferation and inducing cells apoptosis.