Fig. 2

Targeting SETD8 sensitizes cisplatin treatmentin vitro. (A) Distribution of SETD8 and other high-frequency mutant genes in chemotherapy responders and non-responders. (B) Knockdown efficiency of SETD8 siRNAs in SiHa cells. **: p < 0.01. (C) Knockdown efficiency of SETD8 siRNAs in CaSki cells. (D) Dose-response curves of SiHa cells with cisplatin after transfection with two different siSETD8 compared to siNC. IC50 values were derived from the dose-response assay indicating that responsiveness to cisplatin is significantly increased in SiHa after transfection with siSETD8#1 and siSETD8#2. (E) Dose-response curves of CaSki cells to cisplatin after transfection with two different siSETD8 compared to siNC. IC50 values were derived from the dose-response assay. (F) SiHa cells transfected with siNC and siSETD8#1 were treated with 20 µM for 48 h. The apoptotic of SiHa cells were assayed by Annexin V-FITC/PI staining. (G) CaSki cells transfected with siNC and siSETD8#1 were treated with 20 µM for 48 h. The apoptotic of CaSki cells were assayed by Annexin V-FITC/PI staining. Error bars represent ± SD from three replicates. p values were determined by two-tailed Student’s t test (ns: not significant; *: 0.01 ≤ p < 0.05; **: 0.001 ≤ p < 0.01; ***: 0.0001 ≤ p < 0.001; ****: p < 0.0001). (H-I) Colony formation assays were performed using SiHa and CaSki cells with SETD8 knockdown and cisplatin treatment. p values were determined by two-tailed Student’s t test and Fisher’s exact test (ns: not significant; *: 0.01 ≤ p < 0.05; **: 0.001 ≤ p < 0.01; ***: 0.0001 ≤ p < 0.001; ****: p < 0.0001)