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Collapsing the Metabolic PON2zi Scheme in Pancreatic Ductal Adenocarcinoma
Trends in Cell Biology ( IF 19.0 ) Pub Date : 2017-10-04 , DOI: 10.1016/j.tcb.2017.09.003
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.



中文翻译:

胰管腺癌的代谢PON2zi方案崩溃。

胰腺导管腺癌(PDAC)细胞的标志是代谢重编程,可促进肿瘤进展。Nagarajan等人在分子细胞杂志(Molecular Cell)中发表的最新论文中。发现对氧磷酶(PON)2刺激葡萄糖转运蛋白(GLUT)1介导的葡萄糖摄取,阻止AMP激活的蛋白激酶(AMPK)介导的失神经,从而促进PDAC的发展和转移。

更新日期:2017-10-04
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