ArticleFrontiers in oncology2023
Methylation of the epigenetic JMJD2D protein by SET7/9 promotes prostate tumorigenesis.
Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Promotion of breast cancer by the DNPH1 enzyme.iScience · 2026Article
- Anti-tumor activity of CDYL2b in prostate cancer.Cancer letters · 2025Article
- Histone demethylase JMJD2D emerges as a novel prognostic biomarker and exhibits correlation with immune infiltration in lung adenocarcinoma.Discover oncology · 2025Article
- Targeting N-Methyl-lysine Histone Demethylase KDM4 in Cancer: Natural Products Inhibitors as a Driving Force for Epigenetic Drug Discovery.ChemMedChem · 2025Review
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Abstract
How the function of the JMJD2D epigenetic regulator is regulated or whether it plays a role in prostate cancer has remained elusive. We found that JMJD2D was overexpressed in prostate tumors, stimulated prostate cancer cell growth and became methylated by SET7/9 on K427. Mutation of this lysine residue in JMJD2D reduced the ability of DU145 prostate cancer cells to grow, invade and form tumors and elicited extensive transcriptomic changes. This included downregulation of CBLC, a ubiquitin ligase gene with hitherto unknown functions in prostate cancer, and upregulation of PLAGL1, a transcription factor with reported tumor suppressive characteristics in the prostate. Bioinformatic analyses indicated that
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