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• W2782199221 abstract "// Subhra Dash 1 , Prasad M. Sarashetti 2 , Balaji Rajashekar 2, 3 , Rajdeep Chowdhury 1 and Sudeshna Mukherjee 1 1 Department of Biological Sciences, Birla Institute of Technology and Science (BITS), Pilani, Pilani Campus, Rajasthan, India 2 Genotypic Technology Pvt. Ltd., Bangalore, India 3 Institute of Computer Science, University of Tartu, Estonia Correspondence to: Sudeshna Mukherjee, email: sudeshna@pilani.bits-pilani.ac.in Rajdeep Chowdhury, email: rajdeep.chowdhury@pilani.bits-pilani.ac.in Keywords: autophagy; ROS; EMT; TGF-β2; TNF-α Received: June 16, 2017      Accepted: December 23, 2017      Published: January 04, 2018 ABSTRACT Hepatocellular carcinoma (HCC) typically develops in a chronic inflammatory setting causal to release of a plethora of growth factors and cytokines. However, the molecular effect of these cytokines on HCC progression is poorly understood. In this study, we exposed HCC cells to TGF-β2 (Transforming Growth Factor-β2), which resulted in a significant elevation of EMT (Epithelial to Mesenchymal Transition) like features. Molecular analysis of EMT markers showed an increase at both RNA and protein levels upon TGF-β2 administration along with up-regulation of TGF-β-induced Smad signaling. Induction of EMT was associated with a simultaneous increase in reactive oxygen species (ROS) and cytostasis of TGF-β2-treated cells. Importantly, quenching of ROS resulted in a significant promotion of TGF-β2-induced EMT. Furthermore, cells treated with TGF-β2 also showed an enhanced autophagic flux. Interestingly, inhibition of autophagy by chloroquine-di-phosphate (CQDP) or siRNA-mediated ablation of ATG5 drastically inhibited TGF-β2-induced EMT. Autophagy inhibition significantly increased ROS levels promoting apoptosis. It was further observed that pro-inflammatory cytokine like, TNF-α (Tumor Necrosis Factor-α) can antagonize TGF-β2-induced response by down-regulating autophagy, increasing ROS levels and thus inhibiting EMT in HCC cells. This inhibitory effect of TNF-α is serum-independent. Transcriptomic analysis through RNA sequencing was further performed which validated that TGF-β2-induced autophagic genes are inhibited by TNF-α treatment suppressing EMT. Our study suggests that autophagy plays a pro-metastatic role facilitating EMT by regulating ROS levels in HCC cells and TNF-α can suppress EMT by inhibiting autophagy. We provide unique mechanistic insights into the role of TGF-β2 in HCC cells, along with appropriate cues to effectively control the disease." @default.
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• W2782199221 date "2018-01-04" @default.
• W2782199221 modified "2023-10-16" @default.
• W2782199221 title "TGF-β2-induced EMT is dampened by inhibition of autophagy and TNF-α treatment" @default.
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• W2782199221 doi "https://doi.org/10.18632/oncotarget.23942" @default.
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