ArticleThe Journal of clinical investigation2013
KDM2A promotes lung tumorigenesis by epigenetically enhancing ERK1/2 signaling.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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Who cites it
106 citing papers in PubMed, 196 citations in OpenAlex.
- Kdm2a histone demethylase ablation restores anti-tumor immunogenicity in liver cancer.British journal of cancer · 2026Article
- Structure and mechanism of inhibition of lysine demethylase 2A (KDM2A) by compound 183c.Communications chemistry · 2026Article
- Current Insights and Future Directions of Multiomic and Spatial-Omic Analysis in Non-Small Cell Lung Cancer.JCO precision oncology · 2026Review
- Nuclear-localized metabolic enzymes: emerging key players in tumor epigenetic regulation.Molecular and cellular biochemistry · 2025Review
- Dual-Specificity Protein Phosphatases Targeting Extracellular Signal-Regulated Kinases: Friends or Foes in the Biology of Cancer?International journal of molecular sciences · 2025Review
- Article
- TC2N maintains stem cell-like characteristics to accelerate lung carcinogenesis by blockade of dual specificity protein phosphatase 3.Cell & bioscience · 2025Article
- Macrophage KDM2A promotes atherosclerosis via regulating FYN and inducing inflammatory response.International journal of biological sciences · 2025Article
- KDM5D histone demethylase mediates p38α inactivation via its enzymatic activity to inhibit cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- An RNA damage response network mediates the lethality of 5-FU in colorectal cancer.Cell reports. Medicine · 2024Article
- The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling During Neurodevelopment.Neuroscience bulletin · 2024Article
- The emerging and diverse roles of F-box proteins in spermatogenesis and male infertility.Cell regeneration (London, England) · 2024Review
- Acquired resistance to immunotherapy and chemoradiation in MYC amplified head and neck cancer.NPJ precision oncology · 2024Article
- Hepatitis B virus core protein stabilizes RANGAP1 to upregulate KDM2A and facilitate hepatocarcinogenesis.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Sex differences in the tumor promoting effects of tobacco smoke in a cRaf transgenic lung cancer disease model.Archives of toxicology · 2024Article
- Longitudinal dynamics of the tumor hypoxia response: From enzyme activity to biological phenotype.Science advances · 2023Review
- Article
- Review
- An RNA Damage Response Network Mediates the Lethality of 5-FU in Clinically Relevant Tumor Types.bioRxiv : the preprint server for biology · 2023Article
- The Role of ERK1/2 Pathway in the Pathophysiology of Alzheimer's Disease: An Overview and Update on New Developments.Cellular and molecular neurobiology · 2023Review
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
Abstract
Epigenetic dysregulation has emerged as a major contributor to tumorigenesis. Histone methylation is a well-established mechanism of epigenetic regulation that is dynamically modulated by histone methyltransferases and demethylases. The pathogenic role of histone methylation modifiers in non-small cell lung cancer (NSCLC), which is the leading cause of cancer deaths worldwide, remains largely unknown. Here, we found that the histone H3 lysine 36 (H3K36) demethylase KDM2A (also called FBXL11 and JHDM1A) is frequently overexpressed in NSCLC tumors and cell lines. KDM2A and its catalytic activity were required for in vitro proliferation and invasion of KDM2A-overexpressing NSCLC cells. KDM2A overexpression in NSCLC cells with low KDM2A levels increased cell proliferation and invasiveness. KDM2A knockdown abrogated tumor growth and invasive abilities of NSCLC cells in mouse xenograft models. We identified dual-specificity phosphatase 3 (DUSP3) as a key KDM2A target gene and found that DUSP3 dephosphorylates ERK1/2 in NSCLC cells. KDM2A activated ERK1/2 through epigenetic repression of DUSP3 expression via demethylation of dimethylated H3K36 at the DUSP3 locus. High KDM2A levels correlated with poor prognosis in NSCLC patients. These findings uncover an unexpected role for a histone methylation modifier in activating ERK1/2 in lung tumorigenesis and metastasis, suggesting that KDM2A may be a promising therapeutic target in NSCLC.
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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.