Journal
CELL
Volume 168, Issue 4, Pages 692-706Publisher
CELL PRESS
DOI: 10.1016/j.cell.2016.12.004
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Funding
- Irvington Institute Fellowship Program of the Cancer Research Institute
- Ann Schreiber Mentored Investigator Award of the Ovarian Cancer Research Fund Alliance
- Ovarian Cancer Academy Early-Career Investigator Award of the Department of Defense [W81XWH-16-1-0438]
- Stand Up to Cancer Innovative Research Grant [SU2C-AACR-1RG-03-16]
- Clinic and Laboratory Integration Program of the Cancer Research Institute
- Weill Cornell Medical College Funds
- NIH [R01CA112663]
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Malignant cells utilize diverse strategies that enable them to thrive under adverse conditions while simultaneously inhibiting the development of anti-tumor immune responses. Hostile microenvironmental conditions within tumor masses, such as nutrient deprivation, oxygen limitation, high metabolic demand, and oxidative stress, disturb the protein-folding capacity of the endoplasmic reticulum (ER), thereby provoking a cellular state of ER stress. Sustained activation of ER stress sensors endows malignant cells with greater tumorigenic, metastatic, and drug-resistant capacity. Additionally, recent studies have uncovered that ER stress responses further impede the development of protective anti-cancer immunity by manipulating the function of myeloid cells in the tumor microenvironment. Here, we discuss the tumorigenic and immunoregulatory effects of ER stress in cancer, and we explore the concept of targeting ER stress responses to enhance the efficacy of standard chemotherapies and evolving cancer immunotherapies in the clinic.
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