NLRC4, inflammation and colorectal cancer (Review).
Nod‑like receptor C4
colorectal cancer
mechanism of action
prognosis
signaling pathway
Journal
International journal of oncology
ISSN: 1791-2423
Titre abrégé: Int J Oncol
Pays: Greece
ID NLM: 9306042
Informations de publication
Date de publication:
Oct 2024
Oct 2024
Historique:
received:
09
07
2024
accepted:
19
08
2024
medline:
6
9
2024
pubmed:
6
9
2024
entrez:
6
9
2024
Statut:
ppublish
Résumé
Chronic inflammation is recognized as a major risk factor for cancer and is involved in every phase of the disease. Inflammasomes are central to the inflammatory response and play a crucial role in cancer development. The present review summarizes the role of Nod‑like receptor C4 (NLRC4) in inflammation and colorectal cancer (CRC). Reviews of the literature were conducted using Web of Science, PubMed and CNKI, with search terms including 'NLRC4', 'colorectal cancer', 'auto‑inflammatory diseases' and 'prognosis'. Variants of NLRC4 can cause recessive immune dysregulation and autoinflammation or lead to ulcerative colitis as a heterozygous risk factor. Additionally, genetic mutations in inflammasome components may increase susceptibility to cancer. NLRC4 is considered a tumor suppressor in CRC. The role of NLRC4 in CRC signaling pathways is currently understood to involve five key aspects (caspase 1, NLRP3/IL‑8, IL‑1β/IL‑1, NAIP and p53). The mechanisms by which NLRC4 is involved in CRC are considered to be threefold (through pyroptosis, apoptosis, necroptosis and PANoptosis; regulating the immune response; and protecting intestinal epithelial cells to prevent CRC). However, the impact of NLRC4 mutations on CRC remains unclear. In conclusion, NLRC4 is a significant inflammasome that protects against CRC through various signaling pathways and mechanisms. The association between NLRC4 mutations and CRC warrants further investigation.
Identifiants
pubmed: 39239759
doi: 10.3892/ijo.2024.5687
pii: 99
doi:
pii:
Substances chimiques
NLRC4 protein, human
0
Calcium-Binding Proteins
0
CARD Signaling Adaptor Proteins
0
Inflammasomes
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM