期刊
TRENDS IN CANCER
卷 3, 期 9, 页码 643-658出版社
CELL PRESS
DOI: 10.1016/j.trecan.2017.07.002
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资金
- European Union's Horizon research and innovation programme under the Marie Sklodowska-Curie grant [642295]
- FWO postdoctoral fellowship
- FWO [G060713N, G076617N]
- KU Leuven [C16/15/073]
The unfolded protein response (UPR) is a conserved pathway that is stimulated when endoplasmic reticulum (ER) proteostasis is disturbed or lost. Accumulating evidence indicates that chronic activation of the UPR supports the main hallmarks of cancer by favoring cancer cell-autonomous and nonautonomous processes, which ultimately foster the immunosuppressive and protumorigenic microenvironment. However, certain forms of therapy-induced ER stress can elicit immunogenic cancer cell death (ICD), which enables the release of key immunostimulatory or danger signals, eventually driving efficient antitumor immunity. In this review, after a brief discussion of the interplay between ER stress and protumorigenic inflammation, we review the relevance of therapy-mediated ER stress pathways in evoking ICD and how they could be used to optimize current immunotherapy approaches against cancer.
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