Skip to main content
Fig. 8 | Molecular Cancer

Fig. 8

From: circPARD3 drives malignant progression and chemoresistance of laryngeal squamous cell carcinoma by inhibiting autophagy through the PRKCI-Akt-mTOR pathway

Fig. 8

PRKCI inhibits LSCC cell autophagy via activating the Akt-mTOR axis. a and b The protein levels of PRKCI, LC3B, and p62 in FD-LSC-1 and Tu 177 cells with knockdown (a) or overexpression (b) of PRKCI were detected by Western blotting. c and d mCherry-EGFP-LC3B labeled FD-LSC-1 and Tu 177 cells were transfected with si-PRKCI (c) or infected with PRKCI overexpression lentiviruses (d), autophagic flux was analyzed by confocal microscopy. e PRKCI overexpressing FD-LSC-1 and Tu 177 cells (PRKCI-OE) were treated with MK-2206 (10 μM) or Rapamycin (100 nM) for 24 h, the protein levels of phosphorylated Akt (p-AKT(T308), p-AKT(S473)), phosphorylated mTOR (p-mTOR), LC3B, and p62 were detected by western blotting. f mCherry-EGFP-LC3B labeled FD-LSC-1 and Tu 177 cells were infected with PRKCI overexpression lentiviruses for 48 h, then treated with MK-2206 (10 μM) or Rapamycin (100 nM) for 24 h. Autophagic flux was analyzed by confocal microscopy. Scale bar, 25 μm. Error bars represent SD of three independent experiments. **P < 0.01

Back to article page

Molecular Cancer

ISSN: 1476-4598