Investigation of the effect of estradiol and subculturing on the receptor expression within hormone-dependent breast cancer cells

It is now known that a very crucial role in breast cancer development, prognosis and occurrence is played by the estrogen receptor (ER). The steroid hormone estradiol (E2) acts via two nuclear receptors, estrogen receptor- (ER) and estrogen receptor-{beta} (ER{beta}). E2 was shown previously to increase breast cancer cell proliferation in a dose-dependent manner and also induce apoptosis in long term estrogen deprived breast cancer cells. Studies have also shown that the degree of subculturing affects cell line property including gene expression. The aim of this study was to investigate the effect of E2 concentration on cell proliferation, morphology and ER expression and to investigate the effect of subculturing on the expression of ER. Our results have shown that an increase in E2 concentration was found to increase MCF-7 cell proliferation, but extreme concentrations caused significantly low cell proliferation and induced apoptosis. Moreover, ER expression was significantly upregulated with an increase in E2 concentration, whereas ER{beta}2 expression was found to be unchanged at low E2 concentration and significantly upregulated at higher E2 concentration. ER expression at passage 3 ([E2]=1nM) was significantly downregulated compared to the cells at passage 0, in addition to the significant downregulation of the same at E2 concentrations of 1nM and 10{micro}M compared to the untreated control sample. Overall, our data suggests that high concentration of E2 can reduce proliferation and induce apoptosis in the breast cancer cells. Increased E2 exposure and subculturing also appear to change the ER expression significantly in the breast cancer cell line.