FIGURE 3.

Exogenous overexpression and knockdown of PLAC8 influenced ADM sensitivity in breast cancer cells. A, B. Protein and mRNA expression of PLAC8 in MCF‐7/ADMR transfected with the control siRNA (NC), PLAC8 siRNA (siPLAC8‐1, siPLAC8‐2, siPLAC8‐3). GAPDH was used as a loading control. C. Drug sensitivity test for ADM in MCF‐7/ADMR cells infected with NC or PLAC8 siRNA (siPLAC8‐1, siPLAC8‐2, siPLAC8‐3). Cells were treated with various indicated concentrations of ADM for 48 h; cell viability upon drug treatment was analysed by an MTS assay. D. Colony formation assay were conducted to test cell response to ADM in MCF‐7/ADMR PLAC8 silencing cells, compared to the control group. E, F. Protein and mRNA expression of PLAC8 in MCF‐7 cells transfected with PLAC8 overexpression vector, and C1 and C2 were constructed‐PLAC8 stable expression cell clones. GAPDH was used as a loading control. G. Colony formation assay were conducted to test cell response to ADM in MCF‐7 PLAC8‐overexpressed cells (C1 and C2), compared to the control group. H. Drug sensitivity test for ADM in MCF‐7 cells infected with con vector or PLAC8 overexpression vector (PLAC8 OE). Cells were treated with various indicated concentrations of ADM for 48 h, cell viability upon drug treatment was analysed by an MTS assay. Each bar represents the mean ± SD of three independent experiments. *P < .05, **P < .01, ***P < .001