Collapsing the Metabolic PON2zi Scheme in Pancreatic Ductal Adenocarcinoma

Publication date: Available online 4 October 2017
Source:Trends in Cell Biology
Author(s): Matyas Abel Tsegaye, Zachary T. Schafer
A hallmark of pancreatic ductal adenocarcinoma cancer (PDAC) cells is metabolic reprogramming that facilitates tumor progression. In a recent paper published in Molecular Cell, Nagarajan et al. discover that paraoxonase (PON)2 stimulates glucose transporter (GLUT)1-mediated glucose uptake, prevents AMP-activated protein kinase (AMPK)-mediated anoikis, and consequently promotes PDAC development and metastasis.



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