Journal
CANCER CELL
Volume 30, Issue 6, Pages 925-939Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2016.10.010
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Funding
- NIH [CA109311, CA099031, CCSG CA016672]
- Cancer Prevention Research Institute of Texas [RP160710]
- Patel Memorial Breast Cancer Endowment Fund
- National Breast Cancer Foundation
- Breast Cancer Research Foundation
- University of Texas MD Anderson Cancer Center-China Medical University and Hospital Sister Institution Fund
- Ministry of Science and Technology, International Research-intensive Centers of Excellence in Taiwan (I-RiCE) [MOST 105-2911-1-002-302]
- Ministry of Health and Welfare, China Medical University Hospital Cancer Research Center of Excellence [MOHW105-TDU-B-212-134003]
- Center for Biological Pathways
- Susan G. Komen for the Cure Postdoctoral Fellowship [PDF12231298]
- Basic Science Research Program through the National Research Foundation of Korea - Korean government (MSIP) [NRF-2011-357-C00140]
- National Research Foundation of Korea - Korean government (MSIP) [20110030001]
- STCube Pharmaceuticals, Inc., through the MD Anderson Cancer Center
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Pro-inflammatory cytokines produced in the tumor microenvironment lead to eradication of anti-tumor immunity and enhanced tumor cell survival. In the current study, we identified tumor necrosis factor alpha (INF-alpha) as a major factor triggering cancer cell immunosuppression against T cell surveillance via stabilization of programmed cell death-ligand 1 (PD-L1). We demonstrated that COP9 signalosome 5 (CSN5), induced by NF-kappa B p65, is required for TNF-alpha-mediated PD-L1 stabilization in cancer cells. CSN5 inhibits the ubiquitination and degradation of PD-L1. Inhibition of CSN5 by curcumin diminished cancer cell PD-L1 expression and sensitized cancer cells to anti-CTLA4 therapy.
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