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

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...

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Detalles Bibliográficos
Autores principales: Wang, Hailun, Tran, Phuoc T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2018
Materias:
Author’s Views
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6370387/
https://www.ncbi.nlm.nih.gov/pubmed/30788419
http://dx.doi.org/10.1080/23723556.2018.1543485
Descripción
Sumario: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 Kras(G12D)-driven lung tumorigenesis.

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