ArticleOncology letters2018
A potential common role of the Jumonji C domain-containing 1A histone demethylase and chromatin remodeler ATRX in promoting colon cancer.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 24 citations in OpenAlex.
- DNPH1 exerts context-dependent tumor-promoting and -repressing functions during melanoma development.The Journal of investigative dermatology · 2026Article
- Promotion of breast cancer by the DNPH1 enzyme.iScience · 2026Article
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Anti-tumor activity of CDYL2b in prostate cancer.Cancer letters · 2025Article
- Demystifying the Role of Histone Demethylases in Colorectal Cancer: Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2025Review
- Epigenetic roles of KDM3B and KDM3C in tumorigenesis and their therapeutic implications.Cell death & disease · 2024Review
- Article
- Somatic Copy Number Alterations in Colorectal Cancer Lead to a Differentially Expressed ceRNA Network (ceRNet).Current issues in molecular biology · 2023Article
- SET7/9-mediated methylation affects oncogenic functions of histone demethylase JMJD2A.JCI insight · 2023Article
- Predictive Genetic Biomarkers for the Development of Peritoneal Metastases in Colorectal Cancer.International journal of molecular sciences · 2023Article
- Methylation of the epigenetic JMJD2D protein by SET7/9 promotes prostate tumorigenesis.Frontiers in oncology · 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
- Review
- JMJD family proteins in cancer and inflammation.Signal transduction and targeted therapy · 2022Review
- KDM3A regulates alternative splicing of cell-cycle genes following DNA damage.RNA (New York, N.Y.) · 2021Article
- Sumoylation of transcription factor ETV1 modulates its oncogenic potential in prostate cancer.International journal of clinical and experimental pathology · 2021Article
- Crucial Functions of the JMJD1/KDM3 Epigenetic Regulators in Cancer.Molecular cancer research : MCR · 2021Review
- 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
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Jumonji C domain-containing 1A (JMJD1A) is a histone demethylase and epigenetic regulator that has been implicated in cancer development. In the current study, its mRNA and protein expression was analyzed in human colorectal tumors. It was demonstrated that JMJD1A levels were increased and correlated with a more aggressive phenotype. Downregulation of JMJD1A in human HCT116 colorectal cancer cells caused negligible growth defects, but robustly decreased clonogenic activity. Transcriptome analysis revealed that JMJD1A downregulation led to multiple changes in HCT116 cells, including inhibition of MYC- and MYCN-regulated pathways and stimulation of the TP53 tumor suppressor response. One gene identified to be stimulated by JMJD1A was α-thalassemia/mental retardation syndrome X-linked (ATRX), which encodes for a chromatin remodeler. The JMJD1A protein, but not a catalytically inactive mutant, activated the ATRX gene promoter and JMJD1A also affected levels of dimethylation on lysine 9 of histone H3. Similar to JMJD1A, ATRX was significantly overexpressed in human colorectal tumors and correlated with increased disease recurrence and lethality. Furthermore, ATRX downregulation in HCT116 cells reduced their growth and clonogenic activity. Accordingly, upregulation of ATRX may represent one mechanism by which JMJD1A promotes colorectal cancer. In addition, the data presented in this study suggest that the current notion of ATRX as a tumor suppressor is incomplete and that ATRX might context dependently also function as a tumor promoter.
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