ArticlePloS one2012
Regulation of tumor suppressor p53 and HCT116 cell physiology by histone demethylase JMJD2D/KDM4D.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 75 citations in OpenAlex.
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- Promotion of breast cancer by the DNPH1 enzyme.iScience · 2026Article
- Anti-tumor activity of CDYL2b in prostate cancer.Cancer letters · 2025Article
- The emerging roles of histone demethylases in cancers.Cancer metastasis reviews · 2024Review
- Histone lysine demethylase 4 family proteins maintain the transcriptional program and adrenergic cellular state of MYCN-amplified neuroblastoma.Cell reports. Medicine · 2024Article
- SET7/9-mediated methylation affects oncogenic functions of histone demethylase JMJD2A.JCI insight · 2023Article
- Chromosome-level Asian elephant genome assembly and comparative genomics of long-lived mammals reveal the common substitutions for cancer resistance.Aging cell · 2023Article
- Promotion of colorectal cancer by transcription factor BHLHE40 involves upregulation ofFrontiers in oncology · 2023Article
- Methylation of the JMJD2B epigenetic regulator differentially affects its ability to coactivate the ETV1 and JUN transcription factors.International journal of biochemistry and molecular biology · 2023Article
- Methylation of the epigenetic JMJD2D protein by SET7/9 promotes prostate tumorigenesis.Frontiers in oncology · 2023Article
- Review
- The JMJD Family Histone Demethylases in Crosstalk Between Inflammation and Cancer.Frontiers in immunology · 2022Review
- The chemotherapeutic drug carboplatin affects macrophage responses to LPS and LPS tolerance via epigenetic modifications.Scientific reports · 2021Article
- Histone methylation in pancreatic cancer and its clinical implications.World journal of gastroenterology · 2021Review
- Histone demethylase KDM4C controls tumorigenesis of glioblastoma by epigenetically regulating p53 and c-Myc.Cell death & disease · 2021Article
- KDM4 Involvement in Breast Cancer and Possible Therapeutic Approaches.Frontiers in oncology · 2021Review
- Sumoylation of transcription factor ETV1 modulates its oncogenic potential in prostate cancer.International journal of clinical and experimental pathology · 2021Article
- Overexpression of KDM4D promotes acute myeloid leukemia cell development by activating MCL-1.American journal of translational research · 2021Article
- Cooperation between ETS transcription factor ETV1 and histone demethylase JMJD1A in colorectal cancer.International journal of oncology · 2020Article
- Opposite Roles of the JMJD1A Interaction Partners MDFI and MDFIC in Colorectal Cancer.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
JMJD2D, also known as KDM4D, is a histone demethylase that removes methyl moieties from lysine 9 on histone 3 and from lysine 26 on histone 1.4. Here, we demonstrate that JMJD2D forms a complex with the p53 tumor suppressor in vivo and interacts with the DNA binding domain of p53 in vitro. A luciferase reporter plasmid driven by the promoter of p21, a cell cycle inhibitor and prominent target gene of p53, was synergistically activated by p53 and JMJD2D, which was dependent on JMJD2D catalytic activity. Likewise, overexpression of JMJD2D induced p21 expression in U2OS osteosarcoma cells in the absence and presence of adriamycin, an agent that induces DNA damage. Furthermore, downregulation of JMJD2D inhibited cell proliferation in wild-type and even more so in p53(-/-) HCT116 colon cancer cells, suggesting that JMJD2D is a pro-proliferative molecule. JMJD2D depletion also induced more strongly apoptosis in p53(-/-) compared to wild-type HCT116 cells. Collectively, our results demonstrate that JMJD2D can stimulate cell proliferation and survival, suggesting that its inhibition may be helpful in the fight against cancer. Furthermore, our data imply that activation of p53 may represent a mechanism by which the pro-oncogenic functions of JMJD2D become dampened.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.