Cyclooxygenases and Prostaglandins in Tumor Immunology and Microenvironment of Gastrointestinal Cancer.

Abstract

Chronic inflammation is a known risk factor for gastrointestinal cancer. The evidence that nonsteroidal anti-inflammatory drugs suppress the incidence, growth, and metastasis of gastrointestinal cancer supports the concept that a nonsteroidal anti-inflammatory drug target, cyclooxygenase, and its downstream bioactive lipid products may provide one of the links between inflammation and cancer. Preclinical studies have demonstrated that the cyclooxygenase-2-prostaglandin E2 pathway can promote gastrointestinal cancer development. Although the role of this pathway in cancer has been investigated extensively for 2 decades, only recent studies have described its effects on host defenses against transformed epithelial cells. Overcoming tumor-immune evasion remains one of the major challenges in cancer immunotherapy. This review summarizes the impacts of the cyclooxygenase-2-prostaglandin E2 pathway on gastrointestinal cancer development. Our focus was to highlight recent advances in our understanding of how this pathway induces tumor immune evasion.

• Authors: Dingzhi Wang, Carlos S Cabalag, Nicholas J Clemons, Raymond N DuBois
• Journal: Gastroenterology (Gastroenterology) Vol. 161 Issue 6 Pg. 1813-1829 (12 2021) ISSN: 1528-0012 [Electronic] United States
• PMID: 34606846 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
• Copyright: Crown Copyright © 2021. Published by Elsevier Inc. All rights reserved.

Chemical References

• Antineoplastic Agents
• Cyclooxygenase 2 Inhibitors
• Inflammation Mediators
• Cyclooxygenase 2
• PTGS2 protein, human
• Dinoprostone

Topics

• Animals
• Antineoplastic Agents (therapeutic use)
• Cancer-Associated Fibroblasts (enzymology, immunology)
• Cyclooxygenase 2 (metabolism)
• Cyclooxygenase 2 Inhibitors (therapeutic use)
• Dinoprostone (metabolism)
• Epithelial Cells (enzymology, immunology)
• Gastrointestinal Neoplasms (drug therapy, enzymology, immunology, pathology)
• Humans
• Immunotherapy
• Inflammation Mediators (metabolism)
• Lymphocytes, Tumor-Infiltrating (enzymology, immunology)
• Signal Transduction
• Tumor Escape (drug effects)
• Tumor Microenvironment (immunology)
• Tumor-Associated Macrophages (enzymology, immunology)