PTGS2
Overview
PTGS2 encodes prostaglandin-endoperoxide synthase 2 (COX-2), the inducible cyclooxygenase that produces prostaglandins mediating inflammation. In gastric carcinogenesis, PTGS2 is activated by H. pylori infection through epigenetic remodeling: the histone demethylase KDM4B (JMJD2B) is upregulated and drives H4 acetylation at the CDKN1A (p21) promoter, contributing to PTGS2 activation and sustaining the pro-inflammatory microenvironment that promotes gastric cancer development.
Alterations observed in the corpus
- Activated as part of the KDM4B/PTGS2/CDKN1A axis driven by H. pylori infection; H. pylori upregulates KDM4B histone demethylase and drives H4 acetylation at the CDKN1A promoter, activating PTGS2 (COX-2) and contributing to gastric carcinogenesis PMID:24816255
- COX-2; induced downstream of S1PR2 (taurocholic-acid–activated) via ERK/AKT/NF-kB signaling in cholangiocarcinoma; contributes to suppression of CD8+ T-cell activity and regulatory T cell recruitment PMID:25608663
Cancer types (linked)
- Gastric cancer (STAD): PTGS2 is a mediator of H. pylori-driven gastric carcinogenesis through the KDM4B epigenetic axis; relevant to familial and sporadic gastric cancer pathogenesis PMID:24816255
Co-occurrence and mutual exclusivity
- Functions downstream of KDM4B in the KDM4B/PTGS2/CDKN1A carcinogenic axis activated by H. pylori PMID:24816255
Therapeutic relevance
- COX-2 inhibition has been explored as a chemopreventive strategy in gastric cancer, though no targeted therapy data for PTGS2 in familial gastric cancer is reported in this corpus PMID:24816255
Open questions
- The extent to which PTGS2 upregulation via the KDM4B axis contributes to familial vs. sporadic gastric cancer and whether COX-2 inhibition modifies cancer risk in H. pylori-eradicated patients remain unresolved PMID:24816255
Sources
This page was processed by crosslinker on 2026-05-14. - PMID:25608663
This page was processed by crosslinker on 2026-05-14.