ArticlePloS one2014
Mammalian lysine histone demethylase KDM2A regulates E2F1-mediated gene transcription in breast cancer cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Histone lysine demethylases in breast cancer: molecular mechanisms, biological functions, and therapeutic intervention.Molecular cancer · 2025Review
- Targeting epigenetic regulators to overcome drug resistance in cancers.Signal transduction and targeted therapy · 2023Review
- Review
- Histone demethylase KDM2A: Biological functions and clinical values (Review).Experimental and therapeutic medicine · 2021Review
- Significance of LINC00460 in the progression and prognosis in digestive tract tumors.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021Article
- Lysine Demethylases: Promising Drug Targets in Melanoma and Other Cancers.Frontiers in genetics · 2021Review
- KDM2A Targets PFKFB3 for Ubiquitylation to Inhibit the Proliferation and Angiogenesis of Multiple Myeloma Cells.Frontiers in oncology · 2021Article
- Synovial Mesenchymal Stem Cell-Derived EV-Packaged miR-31 Downregulates Histone Demethylase KDM2A to Prevent Knee Osteoarthritis.Molecular therapy. Nucleic acids · 2020Article
- Combined expression levels of KDM2A and KDM2B correlate with nucleolar size and prognosis in primary breast carcinomas.Histology and histopathology · 2020Article
- Knockdown of KDM2A inhibits proliferation associated with TGF-β expression in HEK293T cell.Molecular and cellular biochemistry · 2019Article
- Lysine-specific demethylase 2A enhances binding of various nuclear factors to CpG-rich genomic DNAs by action of its CXXC-PHD domain.Scientific reports · 2019Article
- Article
- PTEN Physically Interacts with and Regulates E2F1-mediated Transcription in Lung Cancer.Cell cycle (Georgetown, Tex.) · 2018Article
- LINC00460 modulates KDM2A to promote cell proliferation and migration by targeting miR-342-3p in gastric cancer.OncoTargets and therapy · 2018Article
- KDM2A/B lysine demethylases and their alternative isoforms in development and disease.Nucleus (Austin, Tex.) · 2018Review
- Unraveling a tumor type-specific regulatory core underlying E2F1-mediated epithelial-mesenchymal transition to predict receptor protein signatures.Nature communications · 2017Article
- Loss of the chromatin modifier Kdm2aa causes BrafV600E-independent spontaneous melanoma in zebrafish.PLoS genetics · 2017Article
- Downregulation of miRNA-141 in breast cancer cells is associated with cell migration and invasion: involvement of ANP32E targeting.Cancer medicine · 2017Article
- Loss of Kaiso expression in breast cancer cells prevents intra-vascular invasion in the lung and secondary metastasis.PloS one · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
It is established that histone modifications like acetylation, methylation, phosphorylation and ubiquitination affect chromatin structure and modulate gene expression. Lysine methylation/demethylation on Histone H3 and H4 is known to affect transcription and is mediated by histone methyl transferases and histone demethylases. KDM2A/JHDM1A/FBXL11 is a JmjC-containing histone demethylase that targets mono- and dimethylated Lys36 residues of Histone H3; its function in breast cancer is not fully understood. Here we show that KDM2A is strongly expressed in myoepithelial cells (MEPC) in breast cancer tissues by immunohistochemistry. Ductal cells from ductal carcinoma in situ (DCIS) and infiltrating ductal carcinoma (IDC) show positive staining for KDM2A, the expression decreases with disease progression to metastasis. Since breast MEPCs have tumor-suppressive and anti-angiogenic properties, we hypothesized that KDM2A could be contributing to some of these functions. Silencing KDM2A with small interfering RNAs demonstrated increased invasion and migration of breast cancer cells by suppressing a subset of matrix metalloproteinases (MMP-2, -9, -14 and -15), as seen by real-time PCR. HUVEC cells showed increased angiogenic tubule formation ability in the absence of KDM2A, with a concomitant increase in the expression of VEGF receptors, FLT-1 and KDR. KDM2A physically bound to both Rb and E2F1 in a cell cycle dependent manner and repressed E2F1 transcriptional activity. Chromatin immunoprecipitation (ChIP) assays revealed that KDM2A associates with E2F1-regulated proliferative promoters CDC25A and TS in early G-phase and dissociates in S-phase. Further, KDM2A could also be detected on MMP9, 14 and 15 promoters, as well as promoters of FLT1 and KDR. KDM2A could suppress E2F1-mediated induction of these promoters in transient transfection experiments. These results suggest a regulatory role for KDM2A in breast cancer cell invasion and migration, through the regulation of E2F1 function.
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