ArticleOncogenesis2017
Lysine demethylase KDM2A inhibits TET2 to promote DNA methylation and silencing of tumor suppressor genes in breast cancer.
Article in Oncogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 65 citations in OpenAlex.
- Transcriptomic Signature and PROTAC Strategy Revealed Histone Lysine Demethylase as a Target of Anticancer Activity of Deferiprone.ACS omega · 2026Article
- Histone lysine demethylases in breast cancer: molecular mechanisms, biological functions, and therapeutic intervention.Molecular cancer · 2025Review
- TET-mediated 5hmC in breast cancer: mechanism and clinical potential.Epigenetics · 2025Review
- Transcriptomic Signature and PROTAC Strategy Revealed Histone Lysine Demethylase as a Target of Anticancer Activity of Deferiprone.bioRxiv : the preprint server for biology · 2025Article
- Landscape of TET2 Mutations: From Hematological Malignancies to Solid Tumors.Cancer medicine · 2025Review
- Identifying the "stripe" transcription factors and cooperative binding related to DNA methylation.Communications biology · 2024Article
- The emerging roles of histone demethylases in cancers.Cancer metastasis reviews · 2024Review
- In Vitro and In Vivo Preventive Effects of Thymoquinone against Breast Cancer: Role of DNMT1.Molecules (Basel, Switzerland) · 2024Article
- TET Enzymes and 5hmC Levels in Carcinogenesis and Progression of Breast Cancer: Potential Therapeutic Targets.International journal of molecular sciences · 2023Review
- A novel STAT3/ NFκB p50 axis regulates stromal-KDM2A to promote M2 macrophage-mediated chemoresistance in breast cancer.Cancer cell international · 2023Article
- Review
- Tumour suppressor TET2 safeguards enhancers from aberrant DNA methylation and epigenetic reprogramming in ERα-positive breast cancer cells.Epigenetics · 2022Article
- Unconventional protein post-translational modifications: the helmsmen in breast cancer.Cell & bioscience · 2022Review
- Parallel analysis of transcription, integration, and sequence of single HIV-1 proviruses.Cell · 2022Article
- Clinical Significance of TET2 in Female Cancers.Frontiers in bioengineering and biotechnology · 2022Article
- DysregulatedCancers · 2021Review
- Expression pattern and regulatory effect of lysine-specific demethylase 2A gene in clear cell renal cell carcinoma.BMC urology · 2021Article
- Control of Breast Cancer Pathogenesis by Histone Methylation and the Hairless Histone Demethylase.Endocrinology · 2021Review
- Histone demethylase KDM2A: Biological functions and clinical values (Review).Experimental and therapeutic medicine · 2021Review
- The Potential Equivalents ofCancers · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The coupling between DNA methylation and histone modification contributes to aberrant expression of oncogenes or tumor suppressor genes that leads to tumor development. Our previous study demonstrated that lysine demethylase 2A (KDM2A) functions as an oncogene in breast cancer by promoting cancer stemness and angiogenesis via activation of the Notch signaling. Here, we demonstrate that knockdown of KDM2A significantly increases the 5'-hydroxymethylcytosine (5'-hmc) level in genomic DNA and expression of tet-eleven translocation 2 (TET2) in various breast cancer cell lines. Conversely, ectopic expression of KDM2A inhibits TET2 expression in KDM2A-depleted cells suggesting TET2 is a transcriptional repression target of KDM2A. Our results show that KDM2A interacts with RelA to co-occupy at the TET2 gene promoter to repress transcription and depletion of RelA or KDM2A restores TET2 expression. Upregulation of TET2 in the KDM2A-depleted cells induces the re-activation of two TET downstream tumor suppressor genes, epithelial cell adhesion molecule (EpCAM) and E-cadherin, and inhibits migration and invasion. On the contrary, knockdown of TET2 in these cells decreases EpCAM and E-cadherin and increases cell invasiveness. More importantly, TET2 expression is negatively associated KDM2A in triple-negative breast tumor tissues, and its expression predicts a better survival. Taken together, we demonstrate for the first time that TET2 is a direct repression target of KDM2A and reveal a novel mechanism by which KDM2A promotes DNA methylation and breast cancer progression via the inhibition of a DNA demethylase.
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Registered trials
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.