Skip to main content
. 2016 Sep 30;7(45):74132–74151. doi: 10.18632/oncotarget.12356

Figure 4. Inhibition and knockdown of xCT reduce mitochondrial dysfunction-enhanced cisplatin resistance.

Figure 4

(A, B) The SC-M1 cells were treated with oligomycin, cisplatin, and sulfasalazine (SSA) A. or erastin B. for 48 h. (Oligo: oligomycin 1 μg/ml). C. The SC-M1 cells were treated with antimycin A, cisplatin, and SSA for 48 h. The cell viability was determined by SRB assay. D. Western blot analysis of the xCT protein expression in the xCT-silenced SC-M1 cells (sixCT) and the control cells (siRNA for non-target sequence, siScramble, siScr) under oligomycin treatment for 24h. E. Specific siRNA (60 pmol for 4 × 105 cells in a 6-cm dish) against xCT was used to knock down xCT in the SC-M1 cells. The cells were treated with oligomycin and cisplatin for 48 h. F. The SC-M1 cells were treated with oligomycin, cisplatin (2.5 μg/ml) and/or buthionine sulphoximine (BSO, 0.5 mM) for 48 h. The cell viability was determined by SRB assay. Data represent the mean ± SEM of three independent experiments. *p < 0.05, compared to the control group; + p < 0.05, compared to the oligomycin alone group; & p < 0.05, compared to the individual siScr group.