epigallocatechin-3-gallate induces apoptosis through up-regulation of bax and down-regulation of bcl-2 in prostate cancer cell line

Background and aims: epigallocatechin3gallate (egcg) is a polyphenolic compound from green tea, which its anticancer effects on many types of cancers have been confirmed, but the molecular mechanism by which egcg induces apoptosis remains unknown. the aim of the present study was to investigate antiproliferative properties and apoptotic signaling pathway of egcg on pc3 human prostate cancer cells.materials and methods: cytotoxic effect of egcg on prostate cancer cell line (pc3) was evaluated by mtt assay. dapi staining was carried out to determine the morphological appearance of cells. finally, the expression of bax and bcl2 (apoptosisregulating genes) were evaluated by quantitative realtime polymerase chain reaction (pcr).results: cytotoxicity evaluations demonstrated that egcg prevented prostate cancer cells growth in a time and dose depended manner, but the effect of treatment duration is more significant than effect of concentration. cell growth inhibition was found to be accompanied by nucleus condensation or chromatin fragmentations which are signs of apoptosis, as assessed by dapi staining. quantitative realtime pcr results demonstrated that egcg causes upregulation of bax as a proapoptotic protein, and downregulation of bcl-2 as an antiapoptotic protein, thus shifting the bax/bcl-2 ratio in favor of apoptosis. conclusions: it is tempting to suggest that consumption of egcg could be an effective strategy to inhibit prostate cancer. our results demonstrated that increase in the ratio of bax/bc-2, is the probable molecular mechanisms through which egcg induces apoptosis in pc3 cells.