RÉSUMÉ
AIM: To research different effects of human breast carcinoma cells with different estrogen receptor expressing by antidiabetic drug metformin, and preliminary explore the possible underlying molecular mechanisms. METHODS: Cells were treated with metformin. Growth inhibition rates of the cells were measured by MTT assay. Cell cycle and apoptosis were detected by flow cytometery (FCM). Expressions of HIF-1α mRNA in the cells were measured by RT-PCR. RESULTS: After drug intervention, the cell proliferation were inhibited by metformin, and reinforced with the concentration and reaction time increase (P<0.05). The growth inhibition rates of MCF-7(ER(+);) breast carcinoma cell were higher than MDA-MB-231(ER(-);) breast carcinoma cell at each concentration group (P<0.05). The results of FCM prompted: MCF-7(ER(+);) breast carcinoma cell was arrested in G1 phase by metformin significantly in a dose-dependent increase(P<0.05). While for MDA-MB-231(ER(-);) breast carcinoma cell, only the 20 and 40 mmol/L groups had significant difference compared with the control group(P<0.05); and the percentage of G1 phase arresting were lower than MCF-7(ER(+);) breast carcinoma cell at the same concentration group(P<0.05). The effect of apoptosis for these two kinds of cells via metformin were not obvious(P<0.05). The expressions of HIF-1α mRNA detected by RT-PCR prompted: the expressions of HIF-1α mRNA for these two breast carcinoma cells were in a dose-dependent decrease(P<0.05). CONCLUSION: The effect of metformin for human breast carcinoma cell with estrogen receptor was better than the one without estrogen receptor. Maybe the molecular mechanism had a relationship with HIF-1α up-regulating.