Fig. 7

miR-32-5p increased cisplatin-resistance of prostate cancer via inhibition of the KLF4-BIK axis. a-d miR-32-5p was transfected into PC3 and DU145 cells. The cells were treated with 20 μM cisplatin at the indicated times. Cell apoptosis was analysed by western blotting and cell viability was measured by a CCK8 assay. The expression levels of miR-32-5p were detected by q-RT-PCR. Data represent the mean ± SD of three independent experiments. e-g miR-32-5p inhibitor was transfected into PC3 and DU145 cells. The cells were treated with 20 μM cisplatin as indicated times. Cell apoptosis was analysed by western blotting. Cell viability was detected by a CCK8 assay. Data represent the mean ± SD of three independent experiments. ***p < 0.001 vs. control. h-k Flag-KLF4 or Flag-BIK was transfected into PC3 cells with or without miR-32-5p overexpression. The cells were treated with 20 μM cisplatin at the indicated times. Cell apoptosis was analysed by western blotting. Cell viability was detected by a CCK8 assay. Data represent the mean ± SD of three independent experiments. ***p < 0.001 vs. control