Mechanism of EGCG promoting apoptosis of MCF-7 cell line in human breast cancer.

The aim of the present study was to investigate the effects of epigallocatechin-3-gallate (EGCG) on the apoptosis of the human MCF-7 cancer cell line and the underlying mechanism. MCF-7 cells were divided into the control group and EGCG groups. The proliferation of MCF-7 cells in the two groups was determined using MTT and apoptosis was examined using flow cytometry. Western blot analysis and qRT-PCR were used to analyze P53 and Bcl-2 expression levels. The silencing effect of specific siRNA was evaluated using RT-PCR and western blot analysis. P53 and Bcl-2 expression levels were determined using western blot analysis in the si-P53, EGCG and EGCG-combined si-P53 groups. EGCG inhibited the proliferation of MCF-7 cells in a concentration-dependent manner and IC50 was 37.681 mol/l. The apoptotic rates were 1.37 and 5.83% (t=8.9, p=0.0124) in the blank control and treatment groups after treatment with 30 µmol/l EGCG. The RT-qPCR and western blot results demonstrated that the effect of siRNA interference was evident. The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group. The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group. In conclusion, EGCG suppressed the proliferation of human MCF-7 breast cancer cells and promoted apoptosis. In addition, the underlying mechanism may be related to the P53/Bcl-2 signaling pathway.