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p58(IPK)-mediated attenuation of the proapoptotic PERK-CHOP pathway allows malignant progression upon low glucose.

Abstract：

:As solid tumors expand, oxygen and nutrients become limiting owing to inadequate vascularization and diffusion. How malignant cells cope with this potentially lethal metabolic stress remains poorly understood. We found that glucose shortage associated with malignant progression triggers apoptosis through the endoplasmic reticulum (ER) unfolded protein response (UPR). ER stress is in part caused by reduced glucose flux through the hexosamine pathway. Deletion of the proapoptotic UPR effector CHOP in a mouse model of K-ras(G12V)-induced lung cancer increases tumor incidence, strongly supporting the notion that ER stress serves as a barrier to malignancy. Overcoming this barrier requires the selective attenuation of the PERK-CHOP arm of the UPR by the molecular chaperone p58(IPK). Furthermore, p58(IPK)-mediated adaptive response enables cells to benefit from the protective features of chronic UPR. Altogether, these results show that ER stress activation and p58(IPK) expression control the fate of malignant cells facing glucose shortage.

journal_name

Mol Cell

journal_title

Molecular cell

authors

Huber AL,Lebeau J,Guillaumot P,Pétrilli V,Malek M,Chilloux J,Fauvet F,Payen L,Kfoury A,Renno T,Chevet E,Manié SN

doi

10.1016/j.molcel.2013.01.009

subject

Has Abstract

pub_date

2013-03-28 00:00:00

pages

1049-59

issue

6

eissn

1097-2765

issn

1097-4164

pii

S1097-2765(13)00042-7

journal_volume

49

pub_type

杂志文章

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