Fig. 5

PLOD2 participates in TGF-β1-induced EMT by promoting the nuclear entry of β-catenin. a A Western blot showing an increase in PLOD2 expression after treatment with human TGF-β1 (concentration ranging from 0.2 to 10 ng/ml). The increase in p-AKT relative to total AKT was used to confirm the activation of TGF-β signalling. b Knockdown of PLOD2 attenuated TGF-β1-induced changes in EMT phenotype markers. Control cells and cells transfected with siPLOD2 treated with human TGF-β1 (10 ng/ml) for 72 h were subjected to Western blotting to detect EMT phenotype markers; β-actin was used as a loading control. c The depletion of PLOD2 inhibits the nuclear translocation of β-catenin induced by TGF-β1. After 72 h of treatment with TGF-β1, control cells exhibited strong β-catenin nuclear accumulation (red), whereas β-catenin accumulated in the membranes of siPLOD2 cells. DAPI was used to indicate nuclei (blue). Photos were captured under an oil lens (×1000)