Fig. 9

Overexpression of PRKCI reverses phenotype changes induced by circPARD3 knockdown. a and b The protein levels of phosphorylated Akt (p-AKT(T308), p-AKT(S473)), and phosphorylated mTOR (p-mTOR) in FD-LSC-1 and Tu 177 cells with knockdown (a) or overexpression (b) of circPARD3 were determined by western blotting. c and d mCherry-EGFP-LC3B labeled FD-LSC-1 (c) and Tu 177 (d) cells were transfected with si-circPARD3 alone or transfected with si-circPARD3 and infected with PRKCI overexpression lentiviruses for 48 h, autophagic flux was analyzed by confocal microscopy. Scale bar, 25 μm. e and f FD-LSC-1 and Tu 177 cells were transfected with si-circPARD3 alone or transfected with si-circPARD3 and infected with PRKCI overexpression lentiviruses, cell proliferation was evaluated by colony formation assays (e) and CCK8 analysis (f). g The migration and invasion abilities of FD-LSC-1 and Tu 177 cells with circPARD3 knockdown alone or circPARD3 knockdown and PRKCI overexpression were detected by Transwell assays. Scale bar, 200 μm. h FD-LSC-1 and Tu 177 cells were transfected with si-circPARD3 alone or transfected with si-circPARD3 and infected with PRKCI overexpression lentiviruses for 48 h, then treated with various concentrations of Cisplatin for 24 h. Cell viability was determined by CCK8 assays. Error bars represent SD of three independent experiments. **P < 0.01