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Updated: Aug 2, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Author's view: epithelial plasticity metabolically reprograms normal cells towards a neoplastic-prone state
Hailun Wang1, Phuoc T Tran1,2,3
1Radiation Oncology and Molecular Radiation Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Abstract:
We have uncovered that epithelial plasticity programs metabolically reprogram epithelial lung cells by increasing expression of genes (e.g., glutamine-fructose-6-phosphate transaminase 2 - GFPT2 and UDP-N-acetylglucosamine pyrophosphorylase 1 - UAP1) critical for the hexosamine biosynthetic pathway (HBP) and elevating global protein O-GlcNAcylation - a specific type of glycosylation. We found that increased O-GlcNAcylation could suppress oncogene-induced senescence tumor suppressor pathways that ultimately led to accelerated KrasG12D -driven lung tumorigenesis.
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