Objective:hER-α36 is a variant of estrogen receptor-α,identified and cloned by a team of American.This research is to determine whether hER-α36 can enhance or weaken chemosensitivity to docetaxel in breast cancer cell line MCF-7(ERα66 positive). Methods:RT-PCR was used to detect the expressions of ERα66 and ERα36 in the two human breast cancer cell lines MCF-7(MCF-7/ERα66) and MCF-7 transfected with ERα36(MCF-7/ERα36).The two cell lines were treated with docetaxel(0～100μmol/L),and cell growth and apoptosis were evaluated using MTT(3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyl tetrazolium bromide) assay(using adriamycin(0～50μmol/L) as the control) and flowcytometry. Western blot analysis was used to measure the effect of docetaxel on phosphor-ERK1/2 expression in the two cell lines. Results:The expressions of ERα36 and ERα66 were detectable in both MCF-7/ERα66 and MCF-7/ERα36 cell lines,while the expression of ERα36 in MCF-7/ER36 cells was higher.Both docetaxel and adriamycin inhibited the proliferation of both cells lines in a dose and time dependent manner.In comparison with MCF-7/ERα36 cell line, the MCF-7/ERα66 cells produced greater growth inhibition and apoptosis after treatment with docetaxel,but there was no significant difference in growth inhibition between the two cell lines treated with adriamycin;The MCF-7/ERα36 cell line resulted in a significant activation(phosphorylation) of ERK1/2 after treatment with docetaxel in a dose-dependent manner,but in the MCF-7/ERα66 cell line,a decrease in the level of phosphor-ERK1/2 expression was observed as the dose of docetaxel increased. Conclusion:ERα36 may be an agent that weakens chemosensitivity to docetaxel in breast cancer,probably by activating the expression of ERK1/2. Objective: hER-α36 is a variant of estrogen receptor-α, identified and cloned by a team of American. This research is to determine whether hER-α36 can enhance or weaken chemosensitivity to docetaxel in breast cancer cell line MCF-7 (ERα66 positive ). Methods: RT-PCR was used to detect the expressions of ERα66 and ERα36 in the two human breast cancer cell lines MCF-7 (MCF-7 / ERα66) and MCF-7 transfected with ERα36 (MCF-7 / ERα36). The two cell lines were treated with docetaxel (0-100 μmol / L), and cell growth and apoptosis were evaluated as MTT (3- (4,5-dimethylthiazol- 2-yl) -2,5-diphenyl tetrazolium bromide assay Using adriamycin (0-50 μmol / L) as the control) and flowcytometry. Western blot analysis was used to measure the effect of docetaxel on phosphor-ERK1 / 2 expression in the two cell lines. Results: The expressions of ERα36 and ERα66 were detectable in both MCF-7 / ERα66 and MCF-7 / ERα36 cell lines, while the expression of ERα36 in MCF-7 / ER36 cells was higher. Both docetaxel and adri amycin inhibited the proliferation of both cells lines in a dose and time dependent manner ..In with MCF-7 / ERα36 cell line, the MCF-7 / ERα66 cells produced greater growth inhibition and apoptosis after treatment with docetaxel, but there was no significant difference in growth inhibition between the two cell lines treated with adriamycin; The MCF-7 / ERα36 cell line resulted in a significant activation (phosphorylation) of ERK1 / 2 after treatment with docetaxel in a dose-dependent manner, but in the MCF-7 ERα36 may be an agent that weakens chemosensitivity to docetaxel in breast cancer, probably by activating the expression of ERK1 / 2.