Figures & data
Figure 1. Elevation of WDR62 in oxaliplatin-resistant CRC. (a)TIMER showed that WDR62 was significantly up-regulated in CRC tissues compared to normal tissues. (b)UALCAN showed that WDR62 was significantly up-regulated in CRC tissues compared to normal tissues. (c) GEPIA showed that WDR62 was significantly up-regulated in CRC tissues compared to normal tissues. (d) Exposure to increasing concentrations of oxaliplatin increased IC50 values of oxaliplatin on HCT116 or HT29. (e) The mRNA expression of WDR62 was up-regulated in HCT116/R and HT29/R compared to HCT116 and HT29 cells. (f) Protein expression of WDR62 was up-regulated in HCT116/R and HT29/R compared to HCT116 and HT29 cells. *** vs. HCT116, p < 0.001. ### vs. HT29, p < 0.001.
Figure 2. WDR62 contributed to oxaliplatin resistance in CRC. (a) HCT116/R and HT29/R cells were transfected with shWDR62-1# or shWDR62-2# to reduce the expression of WDR62. (b) Transfection with shWDR62-2# decreased the IC50 values of oxaliplatin on HCT116/R or HT29/R cells. (c) Transfection with shWDR62-2# reduced the cell proliferation of HCT116/R and HT29/R cells. (d) Transfection with shWDR62-2# promoted cell apoptosis of of HCT116/R and HT29/R cells. * p < 0.05, *** p < 0.001.
Figure 3. WDR62 contributed to DNA damage repair in oxaliplatin-resistant CRC. (a) Transfection with shWDR62-2# up-regulated the foci of γ-H2AX expression in HCT116/R and HT29/R cells. (b) Transfection with shWDR62-2# down-regulated protein expression of p-DNA-PK and Rad51 in HCT116/R and HT29/R cells. ** p < 0.01, *** p < 0.001.
Figure 4. WDR62 contributed to activation of MAPK signaling in oxaliplatin-resistant CRC. Transfection with shWDR62-2# down-regulated protein expression of p-ERK, p-JNK, and p-p38 in HCT116/R and HT29/R cells. ** p < 0.01, *** p < 0.001.
Figure 5. WDR62 regulated MAPK signaling in oxaliplatin-resistant CRC. (a) Inhibition of MAPK aggravated WDR62 silencing-induced decrease of cell proliferation in HCT116/R and HT29/R cells. (b) Inhibition of MAPK aggravated WDR62 silence-induced increase of cell apoptosis in HCT116/R and HT29/R cells. (c) Inhibition of MAPK aggravated WDR62 silence-induced increase ofγ-H2AX foci in HCT116/R and HT29/R cells. (d) Inhibition of MAPK aggravated WDR62 silence-induced decrease of p-DNA-PK and Rad51 in HCT116/R and HT29/R cells. * p < 0.05, ** p < 0.01, *** p < 0.001.
