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Activated ERBB2/Her2 licenses sensitivity to apoptosis upon endoplasmic reticulum stress through a PERK-dependent pathway
Journal article   Open access   Peer reviewed

Activated ERBB2/Her2 licenses sensitivity to apoptosis upon endoplasmic reticulum stress through a PERK-dependent pathway

Rosa Martín-Pérez, Carmen Palacios, Rosario Yerbes, Ana Cano-González, Daniel Iglesias-Serret, Joan Gil, Mauricio J Reginato and Abelardo López-Rivas
Cancer research (Chicago, Ill.), v 74(6), pp 1766-1777
15 Mar 2014
PMID: 24453000
url
https://doi.org/10.1158/0008-5472.CAN-13-1747View
Published, Version of Record (VoR) Open

Abstract

ER stress mTOR TRAIL-R2 Akt ERBB2 ERK
HER2/Neu/ERBB2 is a receptor tyrosine kinase overexpressed in approximately 20% of human breast tumors. Truncated or mutant isoforms which show increased oncogenicity compared to the wild-type receptor are found in many breast tumors. Here we report that constitutively active ERBB2 sensitizes human breast epithelial cells to agents that induce endoplasmic reticulum (ER) stress, altering the unfolded protein response (UPR) of these cells. Deregulation of the ERK, AKT and mTOR activities elicited by mutant ERBB2 were involved in mediating this differential UPR response, elevating the response to ER stress and apoptotic cell death. Mechanistic investigations revealed that the increased sensitivity of mutant ERBB2-expressing cells to ER stress relied upon a UPR effector signaling involving the PERK-ATF4-CHOP pathway, upregulation of the proapoptotic cell surface receptor TRAIL-R2 and activation of proapoptotic caspase-8. Collectively, our results offer a rationale for the therapeutic exploration of treatments inducing ER stress against mutant ERBB2-expressing breast tumor cells.

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Web of Science research areas
Oncology
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