期刊
TRENDS IN CANCER
卷 2, 期 5, 页码 252-262出版社
CELL PRESS
DOI: 10.1016/j.trecan.2016.03.007
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类别
资金
- FONDECYT [3160461, 1140549]
- Institut National du Cancer (INCa)
- La Ligue Contre le Cancer
- Millennium Institute [P09-015-F]
- FONDAP [15150012]
- Frick Foundation [20014-15]
- ALS Therapy Alliance [2014-F-059]
- Muscular Dystrophy Association [382453]
- Michael J. Fox Foundation for Parkinson's Research [9277]
- COPEC-UC Foundation [2013.R.40]
- Office of Naval Research-Global (ONR-G) [N62909-16-1-2003]
- CDMRP Amyotrophic Lateral Sclerosis Research Program (ALSRP) Therapeutic Idea Award [AL150111]
- CONICYT fellowship
- [Ecos-ConicytC13S02]
- [CONICYT-USA2013-0003]
Tumor cells are often exposed to intrinsic and external factors that alter protein homeostasis, thus producing endoplasmic reticulum (ER) stress. To cope with this, cells evoke an adaptive mechanism to restore ER proteostasis known as the unfolded protein response (UPR). The three main UPR signaling branches initiated by IRE1 alpha, PERK, and ATF6 are crucial for tumor growth and aggressiveness as well as for microenvironment remodeling or resistance to treatment. We provide a comprehensive overview of the contribution of the UPR to cancer biology and the acquisition of malignant characteristics, thus highlighting novel aspects including inflammation, invasion and metastasis, genome instability, resistance to chemo/radiotherapy, and angiogenesis. The therapeutic potential of targeting ER stress signaling in cancer is also discussed.
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