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Fig. 10 | Molecular Cancer

Fig. 10

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

Fig. 10

circPARD3 inhibits autophagy of LSCC cells via the PRKCI-Akt-mTOR pathway. a FD-LSC-1 and Tu 177 cells with circPARD3 overexpression (circPARD3-OE) were treated with MK-2206 (10 μM) or Rapamycin (100 nM) for 24 h, then the protein levels of phosphorylated Akt (p-AKT(T308), p-AKT(S473)), phosphorylated mTOR (p-mTOR), LC3B, and p62 were detected by western blotting. b and c mCherry-EGFP-LC3B labeled FD-LSC-1 and Tu 177 cells were infected with circPARD3 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. Representative confocal microscopy images (b) and quantitative data (c) were shown. Scale bar, 25 μm. d and e FD-LSC-1 and Tu 177 cells were transfected with si-circPARD3 for 24 h, then cells were treated with Akt activator SC79 (5 μg/ml) (d) or mTOR activator MHY1485 (10 μM) (e) 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. Error bars represent SD of three independent experiments. **P < 0.01

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