The Paradox of the Unfolded Protein Response in Cancer

被引：2

作者：

Vandewynckel, Yves-Paul ^{[1
]}

Laukens, Debby ^{[1
]}

Geerts, Anja ^{[1
]}

Bogaerts, Eliene ^{[1
]}

Paridaens, Annelies ^{[1
]}

Verhelst, Xavier ^{[1
]}

Janssens, Sophie ^{[3
,4
,5
]}

Heindryckx, Femke ^{[2
]}

Van Vlierberghe, Hans ^{[1
]}

机构：

[1] Univ Ghent, Dept Gastroenterol & Hepatol, B-9000 Ghent, Belgium

[2] Uppsala Univ, Dept Med Biochem & Microbiol, Uppsala, Sweden

[3] Univ Ghent, GRP ID Consortium, B-9000 Ghent, Belgium

[4] Univ Hosp, Ghent, Belgium

[5] VIB, Inflammat Res Ctr, Unit Immunoregulat & Mucosal Immunol, Ghent, Belgium

来源：

ANTICANCER RESEARCH | 2013年 / 33卷 / 11期

关键词：

Cancer; endoplasmic reticulum; stress; unfolded protein response; molecular chaperones; activating transcription factor 6; PERK kinase; inositol requiring enzyme-1; review; ENDOPLASMIC-RETICULUM-STRESS; TUMOR-GROWTH; TRANSCRIPTION FACTOR; CHAPERONE GRP78/BIP; REGULATOR GRP78/BIP; CELL-PROLIFERATION; BAX INHIBITOR-1; ACTIVATION; EXPRESSION; INDUCTION;

D O I：

暂无

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The endoplasmic reticulum (ER) is an elaborate organelle that is essential for cellular function and survival. Conditions that interfere with ER functioning can lead to the accumulation of unfolded proteins, which are detected by transmembrane sensors that then initiate the unfolded protein response (UPR) to restore ER proteostasis. If the adaptive response fails, apoptotic cell death ensues. Many studies have focused on how this failure initiates apoptosis, particularly because ER stress-induced apoptosis is implicated in the pathophysiology of several diseases, including cancer. Whether the UPR inhibits tumour growth or protects tumour cells by facilitating their adaptation to stressful conditions within the tumour microenvironment is unknown, and dissection of the UPR network will likely provide answers to this question. In this review, we aim to elucidate the paradoxical role of the UPR in apoptosis and cancer.

引用

页码：4683 / 4694

页数：12

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