ArticleOncotarget2016
Epigenetic silencing of JMJD5 promotes the proliferation of hepatocellular carcinoma cells by down-regulating the transcription of CDKN1A 686.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- KDM8/c-Myc axis-mediated glucose metabolism reprogramming promotes the progression of ovarian cancer.Scientific reports · 2026Article
- JMJD5: a multifunctional regulator in development, homeostasis, and cancer.Frontiers in cell and developmental biology · 2026Review
- DecipheringEpigenomics · 2024Article
- Allyl Isothiocyanate Suppresses the Proliferation in Oral Squamous Cell Carcinoma via Mediating the KDM8/CCNA1 Axis.Biomedicines · 2023Article
- 5-Substituted Pyridine-2,4-dicarboxylate Derivatives Have Potential for Selective Inhibition of Human Jumonji-C Domain-Containing Protein 5.Journal of medicinal chemistry · 2023Article
- Kinetic and inhibition studies on human Jumonji-C (JmjC) domain-containing protein 5.RSC chemical biology · 2023Article
- Histone Demethylation Profiles in Nonalcoholic Fatty Liver Disease and Prognostic Values in Hepatocellular Carcinoma: A Bioinformatic Analysis.Current issues in molecular biology · 2023Article
- Comprehensive analyses of prognostic biomarkers and immune infiltrates among histone lysine demethylases (KDMs) in hepatocellular carcinoma.Cancer immunology, immunotherapy : CII · 2022Article
- The JMJD Family Histone Demethylases in Crosstalk Between Inflammation and Cancer.Frontiers in immunology · 2022Review
- Human 2-oxoglutarate-dependent oxygenases: nutrient sensors, stress responders, and disease mediators.Biochemical Society transactions · 2020Review
- Jumonji domain containing 5 is a potential prognostic indicator in non-small cell lung cancer patients who received platinum-based chemotherapy.Translational cancer research · 2019Article
- Long Noncoding RNA MPRL Promotes Mitochondrial Fission and Cisplatin Chemosensitivity via Disruption of Pre-miRNA Processing.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Dual prognostic role of 2-oxoglutarate-dependent oxygenases in ten cancer types: implications for cell cycle regulation and cell adhesion maintenance.Cancer communications (London, England) · 2019Article
- The small members of the JMJD protein family: Enzymatic jewels or jinxes?Biochimica et biophysica acta. Reviews on cancer · 2019Review
- KDM8/JMJD5 as a dual coactivator of AR and PKM2 integrates AR/EZH2 network and tumor metabolism in CRPC.Oncogene · 2019Article
- Ginsenoside Rh2 inhibits prostate cancer cell growth through suppression of microRNA-4295 that activates CDKN1A.Cell proliferation · 2018Article
- JMJD5 is a human arginyl C-3 hydroxylase.Nature communications · 2018Article
- High expression of FLT3 is a risk factor in leukemia.Molecular medicine reports · 2018Article
- New Insights into the Epigenetics of Hepatocellular Carcinoma.BioMed research international · 2017Review
- Depletion of JMJD5 sensitizes tumor cells to microtubule-destabilizing agents by altering microtubule stability.Cell cycle (Georgetown, Tex.) · 2016Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteins that contain jumonji C (JmjC) domains have recently been identified as major contributors to various malignant human cancers through epigenetic remodeling. However, the roles of these family members in the pathogenesis of hepatocellular carcinoma (HCC) are obscure. By mining public databases, we found that the HCC patients with lower JmjC domain-containing protein 5 (JMJD5) expression exhibited shorter survival time. We then confirmed that JMJD5 expression was indeed decreased in HCC specimens, which was caused by the altered epigenetic histone modifications, the decreased H3K9ac, H3K27ac and H3K4me2/3 together with the increased trimethylation of H3K27 and H3K9 on the JMJD5 promoter. Functional experiments revealed that JMJD5 knockdown promoted HCC cell proliferation and in vivo tumorigenicity by accelerating the G1/S transition of the cell cycle; in contrast, ectopic JMJD5 expression had the opposite effects. At molecular mechanism, we found that, in HCC cell lines including TP53-null Hep3B, JMJD5 knockdown led to the down-regulation of CDKN1A and ectopic expression of JMJD5 not only increased but also rescued CDKN1A transcription. Moreover, CDKN1A knockdown could abrogate the effect of JMJD5 knockdown or overexpression on cell proliferation, suggesting that JMJD5 inhibits HCC cell proliferation mainly by activating CDKN1A expression. We further revealed that JMJD5 directly enhances CDKN1A transcription by binding to CDKN1A's promoter independent of H3K36me2 demethylase activity. In short, we first prove that JMJD5 is a tumor suppressor gene in HCC pathogenesis, and the epigenetic silencing of JMJD5 promotes HCC cell proliferation by directly down-regulating CDKN1A transcription.
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