Estrogen receptor (ER)-negative breast carcinomas are often difficult to treat with antiestrogens. This work was performed to determine if the re-expression of the human ERα could restore the hormone response of these cells. We have transfected the human wild-type ERα to an ER-negative breast cancer cell line (MDA-MB-231) using a tetracycline-regulated gene expression system. We obtained a new cell line, MDA-A4-5/2. Cell count and flow cytometry "S" phase cell fraction showed that 17-β-estradiol induced an inhibition on the proliferation of these cells; on the contrary, the antiestrogens ICI 182 780, and tamoxifen blocked this effect. Finally, we demonstrated an induction of the endogenous progesterone receptor gene when ERα was present. These results suggest that the re-expression of ERα in ER-negative breast cancer cells recreate, at least partially, a hormone-responsive phenotype and may be useful as a therapeutic approach to control this pathology.Key words: human breast carcinoma, MDA-MB-231 cells, estrogen receptor α, tetracycline-regulated gene expression system, cell proliferation.
Human estrogen receptor-α (ER-α) transactivation by selective estrogen receptor modulators (SERMs) on VIT regulatory region in ER-α-negative breast cancer cell line Evsa-T transiently transfected by ER-α
