Journal
TRENDS IN CANCER
Volume 3, Issue 1, Pages 28-38Publisher
CELL PRESS
DOI: 10.1016/j.trecan.2016.12.003
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Funding
- NIH [R01DK074738]
- Broad Foundation [IBD-0328]
- National Multiple Sclerosis Society [PP1779]
- CSTR
- TAM Genomics
- CTEHR
- Sumitomo Life Welfare and Culture Foundation
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Cancer cells need to escape immune surveillance for successful tumor growth. Loss of MHC class I has been described as a major immune evasion strategy in many cancers. MHC class I transactivator (CITA), NLRC5 [nucleotide-binding domain and leucine-rich repeats containing (NLR) family, caspase activation and recruitment domain (CARD) domain containing 5], is a key transcription coactivator of MHC class I genes. Recent genetic studies have revealed that NLRC5 is a major target for cancer immune evasion mechanisms. The reduced expression or activity of NLRC5 caused by promoter methylation, copy number loss, or somatic mutations is associated with defective MHC class I expression, impaired cytotoxic T cell activation, and poor patient prognosis. Here, we review the role of NLRC5 in cancer immune evasion and the future prospects for cancer research.
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