Author's view: epithelial plasticity metabolically reprograms normal cells towards a neoplastic-prone state

Molecular & Cellular Oncology
Hailun Wang, Phuoc T Tran

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.

References

Sep 15, 1999·Genes & Development·R MaestroG J Hannon
Dec 1, 2005·Science's STKE : Signal Transduction Knowledge Environment·Dona C Love, John A Hanover
Dec 8, 2009·Proceedings of the National Academy of Sciences of the United States of America·Per HydbringLars-Gunnar Larsson
Jun 24, 2014·Nature Reviews. Molecular Cell Biology·Daniel Muñoz-Espín, Manuel Serrano
Aug 22, 2018·The Journal of Clinical Investigation·Kekoa TaparraPhuoc T Tran

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Methods Mentioned

BETA
glycosylation
glycosylations

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