Collapsing the Metabolic PON2zi Scheme in Pancreatic Ductal Adenocarcinoma

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...

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Veröffentlicht in:Trends in cell biology 2017-11, Vol.27 (11), p.785-786
Hauptverfasser: Tsegaye, Matyas Abel, Schafer, Zachary T.
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description 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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subjects Adenocarcinoma
AMP
AMP-activated protein kinase
AMP-Activated Protein Kinases
Anoikis
Carcinoma, Pancreatic Ductal
Fluorescence
Glucose
glucose metabolism
Glucose transporter
Glucose transporter 1
Humans
Kinases
Metastases
Metastasis
Pancreas
Pancreatic cancer
pancreatic ductal adenocarcinoma
Paraoxonase
Tumors
title Collapsing the Metabolic PON2zi Scheme in Pancreatic Ductal Adenocarcinoma
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