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The G-Protein Coupled Formyl Peptide Receptors and Their Role in the Progression of Digestive Tract Cancer.

Abstract
Chronic inflammation is a causative factor of many cancers, although it originally acts as a protective host response to the loss of tissue homeostasis. Many inflammatory conditions predispose susceptible cells, most of which are of epithelial origin, to neoplastic transformation. There is a close correlation between digestive tract (DT) cancer and chronic inflammation, such as esophageal adenocarcinoma associated with Barrett's esophagus, helicobacter pylori infection as the cause of stomach cancer, hepatitis leading to liver cirrhosis and subsequent cancer, and colon cancer linking to inflammatory bowel diseases and schistosomiasis. A prominent feature of malignant transformation of DT tract epithelial cells is their adoption of somatic gene mutations resulting in abnormal expression of proteins that endow the cells with unlimited proliferation as well as increased motility and invasive capabilities. Many of these events are mediated by Gi-protein coupled chemoattractant receptors (GPCRs) including formyl peptide receptors (FPRs in human, Fprs in mice). In this article, we review the current understanding of FPRs (Fprs) and their function in DT cancer types as well as their potential as therapeutic targets.
AuthorsCuimeng Tian, Keqiang Chen, Wanghua Gong, Teizo Yoshimura, Jiaqiang Huang, Ji Ming Wang
JournalTechnology in cancer research & treatment (Technol Cancer Res Treat) 2020 Jan-Dec Vol. 19 Pg. 1533033820973280 ISSN: 1533-0338 [Electronic] United States
PMID33251986 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References
  • Biomarkers, Tumor
  • Ligands
  • Receptors, Formyl Peptide
Topics
  • Biomarkers, Tumor
  • Disease Progression
  • Disease Susceptibility
  • Gastrointestinal Neoplasms (genetics, metabolism, pathology)
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Ligands
  • Models, Biological
  • Multigene Family
  • Organ Specificity
  • Protein Binding
  • Receptors, Formyl Peptide (genetics, metabolism)

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