RESUMO
Objective To investigate the effect of STAT3 knockdown on the sensitivity of breast cancer cells with drug-resistant to adriamycin (MCF-7/ADR). Methods Levels of STAT3 and p-STAT3 in MCF-7/ADR and MCF-7 cells were detected by Western Blot. The MCF-7/ADR cells were infected with lentivirus expressing STAT3-shRNA and the negative control vectors in the STAT3-RNAi group and NC group, respectively, wihle the cells in the blank group received no treatment. The transfection efficiency was observed with fluorescence microscope, the mRNA level of STAT3, protein levels of STAT3 and p-STAT3 were detected by qRT-PCR and Western Blot, respectively. MCF-7/ADR cells were treated with different concentrations of adriamycin for 48 hours, cell proliferation was detected by MTT assay and cell apoptosis was detected by flow cytometry. Results Levels of STAT3 and p-STAT3 in MCF-7/ADR cells were significantly higher than those in the MCF-7 cells (P < 0.05). The levels of STAT3 mRNA, STAT3 and p-STAT3 in the STAT3-RNAi group were significantly lower than those in the Con group and the NC group (P<0.05, respectively). The Adriamycin IC50 in the Con group, NC group and STAT3-RNAi group was (56.1 ± 3.00)ug/mL,(54.9 ± 11.9)ug/mL and (7.6 ± 0.2)ug/mL, respectively. The flow cytometry results showed that the cell apoptosis in the Con group, the NC group and the STAT3-RNAi group was (10.5+0.7)%, (11.7+0.7)%and (34+3.1)%, respectively. Conclusion LV-shRNA-STAT3 can significantly inhibit STAT3 expression and enhance the sensitivity of breast cancer cells to adriamycin, and the underlying mechanism may be related to cell apoptosis.