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.
Format:	Artikel
Sprache:	eng
Schlagworte:	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
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Beschreibung
Zusammenfassung:	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.
ISSN:	0962-8924 1879-3088
DOI:	10.1016/j.tcb.2017.09.003