Journal
SEMINARS IN CANCER BIOLOGY
Volume 33, Issue -, Pages 3-15Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2015.04.002
Keywords
ER stress; UPR; Cancer; Tumorigenesis; Therapeutic approaches
Categories
Funding
- National Cancer Institute [1PO1-CA165997]
- NIH [F31CA183569]
- Bodossaki Foundation, Greece
- NATIONAL CANCER INSTITUTE [F31CA183569, P01CA165997] Funding Source: NIH RePORTER
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A variety of cell intrinsic or extrinsic stresses evoke perturbations in the folding environment of the endoplasmic reticulum (ER), collectively known as ER stress. Adaptation to stress and re-establishment of ER homeostasis is achieved by activation of an integrated signal transduction pathway called the unfolded protein response (UPR). Both ER stress and UPR activation have been implicated in a variety of human cancers. Although at early stages or physiological conditions of ER stress, the UPR generally promotes survival, when the stress becomes more stringent or prolonged, its role can switch to a pro-cell death one. Here, we discuss historical and recent evidence supporting an involvement of the UPR in malignancy, describe the main mechanisms by which tumor cells overcome ER stress to promote their survival, tumor progression and metastasis and discuss the current state of efforts to develop therapeutic approaches of targeting the UPR. (C) 2015 Elsevier Ltd. All rights reserved.
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