Autophagy: an emerging key regulator of epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC) cells
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Lung cancer is considered as one of the most important causes of cancer-related death worldwide and Non-Small Cell Lung Cancer (NSCLC) accounts for 80% of all lung cancer cases. Autophagy is a cellular process responsible for the recycling of damaged organelles and protein aggregates. Transforming growth factor beta-1 (TGFβ1) is involved in Epithelial to Mesenchymal Transition (EMT) and autophagy induction in different cancer models and plays an important role in pathogenesis of NSCLC. It is not clear how autophagy can regulate EMT in NSCLC. In the present study, we have investigated the regulatory role of autophagy in EMT induction in NSCLC cells. we showed that TGFβ1 can simultaneously induce both autophagy and EMT. We observed that upon chemical inhibition of autophagy using Bafilomycin-A1 the expression of the mesenchymal marker vimentin is reduced. Also, using immune blotting and immunocytochemistry (ICC) we showed that mesenchymal marker (vimentin) was significantly downregulated upon TGFβ1 treatment in Atg7 knockdown cells compared to corresponding scramble (negative control) cells (**, P<0.01; ***, P<0.001, respectively for A549 and H1975 cells) while E-cadherin was almost unchanged. Also, Atg7 knockdown cells treated with TGFβ1 had less migration (mesenchymal function) compared to scramble counterparts. This study identified a crucial role of autophagy as a potential positive regulator mechanism in the induction of TGFβ1-induced EMT in NSCLC cells.