Fig. 6: TTK depletion inhibits autophagy by activating the mTOR signaling pathway in ovarian cancer cells.

A CAOV3 and OV90 cells were transiently transfected with NC or siTTK for 48 h. Protein levels of LC3-I, LC3-II, TTK, and β-actin were assessed using western blotting. B Western blot assays were conducted to detect the LC3-I, LC3-II, TTK and β-actin protein levels in CAOV3 and OV90 cells after transfection with PCMV or PCMV-TTK. C Representative images of immunofluorescence staining for LC3B in ovarian cancer cells transfected with siTTK, NC, and PCMV-TTK for 48 h (×400). Scale bar: 15 µm. D CAOV3 and OV90 cells transfected with PCMV or PCMV-TTK were treated with or without CQ (50 μM) for 24 h. Levels of the LC3-I, LC3-II, TTK and β-actin proteins were analyzed using western blotting. E CAOV3 and OV90 cells were transfected with NC or siTTK for 48 h. Levels of the p-mTOR, mTOR, TTK, and β-actin proteins were evaluated using western blotting. F Western blot assays were performed to show the levels of the p-mTOR, mTOR, TTK and β-actin proteins in CAOV3 and OV90 cells transfected with PCMV or PCMV-TTK for 48 h. G CAOV3 and OV90 cells transfected with NC or siTTK were treated with or without 100 nM rapamycin for 24 h. The levels of p-mTOR, mTOR, LC3-I/II, TTK, and β-actin were measured using western blotting. H Levels of the LC3-I, LC3-II, TTK, and β-actin proteins in CAOV3 and OV90 cells treated with B389 for 48 h. I Western blot analysis was performed to detect the levels of the p-mTOR, mTOR, TTK and β-actin proteins in CAOV3 and OV90 cells treated with B389 for 48 h (data are mean ± SEM, n = 3).