Oestrogen causes G2/M arrest and apoptosis in breast cancer cells MDA-MB-231.

Flavonoids have been shown to exert many biological activities within cancer cells, and oestrogen is known to be structurally related to flavonoids. We investigated the effects of oestrogen in cancer cells to determine if its activities would be similar to those of flavonoids. When 50 microM 17 beta-oestradiol (oestradiol) was added to the oestrogen receptor (ER) alpha-negative breast cancer cell line MDA-MB-231, growth arrest was apparent, similar to that observed with genistein and daidzein. Oestradiol exhibited a dose response curve for the growth arrest similar to those of genistein and daidzein. Apoptosis occurred in the breast cancer cells after treatment with 50 microM oestradiol, genistein, or daidzein, with similar profiles. Flow cytometry analysis revealed that oestradiol treatment caused G2/M arrest and apoptosis. Cell-cycle arrest at G2/M began at 6 h after treatment, and apoptosis began within 24 h. Because MDA-MB-231 cells are ER alpha negative, these results suggest that oestradiol induces cell-cycle arrest and apoptosis through an ER alpha-independent pathway.