KDM4B
Overview
KDM4B (also known as JMJD2B) encodes a histone lysine demethylase that removes methyl groups from H3K9 and H3K36. In gastric carcinogenesis, H. pylori upregulates KDM4B, leading to epigenetic changes at the CDKN1A (p21) promoter and activation of PTGS2 (COX-2), contributing to the inflammatory-epigenetic cascade underlying gastric cancer development.
Alterations observed in the corpus
- H. pylori upregulates KDM4B (JMJD2B) histone demethylase, driving H4 acetylation at the CDKN1A (p21) promoter and activating PTGS2 (COX-2), contributing to gastric carcinogenesis via an epigenetic-inflammatory axis. PMID:24816255
Cancer types (linked)
- STAD (gastric adenocarcinoma): KDM4B is upregulated by H. pylori infection as part of the epigenetic field defect in pre-cancerous gastric mucosa, contributing to intestinal metaplasia progression. PMID:24816255
Co-occurrence and mutual exclusivity
- Functional axis: KDM4B → H4 acetylation at CDKN1A promoter → PTGS2 (COX-2) activation; all components act downstream of H. pylori infection. PMID:24816255
Therapeutic relevance
- KDM4B inhibition is a potential therapeutic target in H. pylori-driven gastric carcinogenesis; no clinical data reported in this corpus.
Open questions
- Whether KDM4B upregulation in H. pylori-infected mucosa is reversible by eradication, and whether it represents a druggable window in pre-malignant gastric lesions, is unresolved.
Sources
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