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

Figure 2. Inhibition and knockdown of xCT increase the cisplatin sensitivity of cisplatin-resistant gastric cancer cells, and high xCT expression is a poor prognostic factor in gastric cancer patients under adjuvant chemotherapy treatment.

Figure 2

A. The SC-M1CisR cells were treated with cisplatin and SSA for 48 h. The cell viability was determined by MTT assay. B. The SC-M1CisR cells were treated with cisplatin and erastin for 48h. The cell viability was determined by SRB assay. C. Specific siRNA against xCT (60 pmol for 4 × 105 cells in a 6-cm dish) was used to knock down xCT in the SC-M1CisR cells, and the protein level of xCT was analyzed by Western blot analysis. (siRNA for non-target sequence, siScramble, siScr) D. The xCT-silenced SC-M1CisR cells (sixCT) and the control SC-M1CisR cells were treated with cisplatin for 48 h. The cell viability was determined by SRB assay. (E, F) The Kaplan-Meier survival analyses show the effects of xCT expression on overall survival (OS) E. and progression-free survival (PFS) F. in the subgroup of gastric cancer patients (5-FU-based adjuvant gastric cancer patients). Data represent the mean ± SEM of three independent experiments. *p < 0.05, compared to the control group; & p < 0.05, compared to the individual siScr group.