Fig. 6: CK2 regulates cathepsin transportation via IGF2R phosphorylation.

a Proteomic analysis of IGF2R-knockdown cells (SKG-I and CaSki) at 96 h after siRNA transfection. Each fold change value was calculated by digitizing the peak intensity obtained from mass spectrometry. The currently known M6P-labeled protein is colored green. b Co-localization of cathepsins and IGF2R in cervical cancer cells. Parental cells were co-stained with anti-cathepsin B/L (green) and anti-IGF2R (red) antibodies. c Effect of IGF2R knockdown (72 h) on protein expression and processing of cathepsins. Western blotting (upper panel) and densitometry analysis of matured cathepsin B and L expression from three independent experiments (lower panel). d Changes in the intracellular distributions of cathepsins after IGF2R knockdown (72 h). e Effect of CK2 inhibitors on the protein expression and processing of cathepsins. Protein expression in CK2 inhibitor-treated cells (72 h) were analyzed by western blotting. f Dose-response effects of CK2 inhibitors on the cell viability of cervical cancer cells and normal human dermal fibroblasts (NHDFs). Viable cells were detected at 96 hours after the treatment. g Schematic diagram of the biological significance of IGF2R in cervical cancer cells. All the error bars represent the standard deviation of three independent experiments. *p < 0.05, ***p < 0.001; t-test with Welch’s correction and Dunnett’s multiple comparisons test. Scale bars represent 20 μm.