科研之友
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摘要
hER-alpha 36 is a variant of estrogen receptor-alpha, identified and cloned by a team of American. This research is to determine whether hER-alpha 36 can enhance or weaken chemosensitivity to docetaxel in breast cancer cell line MCF-7(ER alpha 66 positive). RT-PCR was used to detect the expressions of ER alpha 66 and ER alpha 36 in the two human breast cancer cell lines MCF-7(MCF-7/ER alpha 66)and MCF-7 transfected with ER alpha 36(MCF-7/ER alpha 36). The two cell lines were treated with docetaxel(0 similar to 100A mu mol/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 similar to 50A mu mol/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. The expressions of ER alpha 36 and ER alpha 66 were detectable in both MCF-7/ER alpha 66 and MCF-7/ER alpha 36 cell lines, while the expression of ER alpha 36 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/ER alpha 36 cell line, the MCF-7/ER alpha 66 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/ER alpha 36 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/ER alpha 66 cell line, a decrease in the level of phosphor-ERK1/2 expression was observed as the dose of docetaxel increased. ER alpha 36 may be an agent that weakens chemosensitivity to docetaxel in breast cancer, probably by activating the expression of ERK1/2.
