NLRC5/CITA: A Key Player in Cancer Immune Surveillance

Trends Cancer. 2017 Jan;3(1):28-38. doi: 10.1016/j.trecan.2016.12.003. Epub 2017 Jan 10.

Abstract

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.

Keywords: CITA; MHC class I; NLRC5; cancer; immune evasion.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Biomarkers, Tumor / immunology
  • Gene Expression Regulation, Neoplastic
  • Genes, MHC Class I
  • Humans
  • Immunologic Surveillance*
  • Intracellular Signaling Peptides and Proteins / immunology*
  • Neoplasms / immunology*
  • Prognosis

Substances

  • Biomarkers, Tumor
  • Intracellular Signaling Peptides and Proteins
  • NLRC5 protein, human