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ATF4-Induced Metabolic Reprograming Is a Synthetic Vulnerability of the p62-Deficient Tumor Stroma.

Abstract：

:Tumors undergo nutrient stress and need to reprogram their metabolism to survive. The stroma may play a critical role in this process by providing nutrients to support the epithelial compartment of the tumor. Here we show that p62 deficiency in stromal fibroblasts promotes resistance to glutamine deprivation by the direct control of ATF4 stability through its p62-mediated polyubiquitination. ATF4 upregulation by p62 deficiency in the stroma activates glucose carbon flux through a pyruvate carboxylase-asparagine synthase cascade that results in asparagine generation as a source of nitrogen for stroma and tumor epithelial proliferation. Thus, p62 directly targets nuclear transcription factors to control metabolic reprogramming in the microenvironment and repress tumorigenesis, and identifies ATF4 as a synthetic vulnerability in p62-deficient tumor stroma.

journal_name

Cell Metab

journal_title

Cell metabolism

authors

Linares JF,Cordes T,Duran A,Reina-Campos M,Valencia T,Ahn CS,Castilla EA,Moscat J,Metallo CM,Diaz-Meco MT

doi

10.1016/j.cmet.2017.09.001

subject

Has Abstract

pub_date

2017-12-05 00:00:00

pages

817-829.e6

issue

6

eissn

1550-4131

issn

1932-7420

pii

S1550-4131(17)30552-1

journal_volume

26

pub_type

杂志文章

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