ArticleEpigenetics2019
Loss of KMT2D induces prostate cancer ROS-mediated DNA damage by suppressing the enhancer activity and DNA binding of antioxidant transcription factor FOXO3.
Article in Epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 59 citations in OpenAlex.
- Genomic analysis of oesophageal carcinoma (EC) identifies recurrent mutations in histone methyltransferases as a distinctive subset.Oncogene · 2026Article
- Histone methyltransferase KMT2D promotes castration-resistant prostate cancer progression by reactivating AR through FOXA1.Oncogene · 2026Article
- Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instability.Nature communications · 2026Article
- Histone methyltransferase KMT2D targets the SPOP-G3BP1 axis to enhance AR stability and drive castration-resistant prostate cancer progression.Molecular biomedicine · 2025Article
- Histone-modifying enzymes as drivers and therapeutic targets in androgen-resistant prostate cancer.Frontiers in endocrinology · 2025Review
- KMT2D-mediated H3K4me1 recruits YBX1 to facilitate triple-negative breast cancer progression through epigenetic activation of c-Myc.Clinical and translational medicine · 2024Article
- Silencing HOXC13 exerts anti-prostate cancer effects by inducing DNA damage and activating cGAS/STING/IRF3 pathway.Journal of translational medicine · 2023Article
- "PRRX1-rearranged mesenchymal tumors": expanding the immunohistochemical profile and molecular spectrum of a recently described entity with the proposed revision of nomenclature.Virchows Archiv : an international journal of pathology · 2023Article
- Review
- Molecular characterization of an embryonal rhabdomyosarcoma occurring in a patient with Kabuki syndrome: report and literature review in the light of tumor predisposition syndromes.Familial cancer · 2023Review
- Pan-Cancer Analysis of Histone Methyltransferase KMT2D with Potential Implications for Prognosis and Immunotherapy in Human Cancer.Combinatorial chemistry & high throughput screening · 2023Article
- Lineage plasticity and treatment resistance in prostate cancer: the intersection of genetics, epigenetics, and evolution.Frontiers in endocrinology · 2023Review
- PLK-1 Interacting Checkpoint Helicase, PICH, Mediates Cellular Oxidative Stress Response.Epigenomes · 2022Article
- Integrated analysis reveals FOXA1 and Ku70/Ku80 as targets of ivermectin in prostate cancer.Cell death & disease · 2022Article
- miR-223 Enhances the Neuroprotection of Estradiol Against Oxidative Stress Injury by Inhibiting the FOXO3/TXNIP Axis.Neurochemical research · 2022Article
- Altered pathways and targeted therapy in double hit lymphoma.Journal of hematology & oncology · 2022Review
- Comprehensive Pan-Cancer Analysis of Senescence With Cancer Prognosis and Immunotherapy.Frontiers in molecular biosciences · 2022Article
- Signature for Prostate Cancer Based on Autophagy-Related Genes and a Nomogram for Quantitative Risk Stratification.Disease markers · 2022Article
- Response prediction biomarkers and drug combinations of PARP inhibitors in prostate cancer.Acta pharmacologica Sinica · 2021Review
- Large-scale analysis of KMT2 mutations defines a distinctive molecular subset with treatment implication in gastric cancer.Oncogene · 2021Article
Corrections and comments
- Erratum issuedCorrection.2021
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone methyltransferase KMT2D has diverse functions and distinct mechanisms in different cancers. Although we have previously found KMT2D serves as an oncogene that promotes tumor growth and metastasis in prostate cancer (PCa), the functions and mechanisms of KMT2D are complicated and most remain undefined. Here, the function of KMT2D regarding DNA damage in PCa and the underlying mechanisms of KMT2D in epigenetic regulation were explored in a series of studies. Knockdown of KMT2D sensitized cells to DNA damage through the disturbance of antioxidative gene expression and increased levels of intracellular reactive oxygen species, which led to cell apoptosis and senescence. The loss of KMT2D reduced the abundance of enhancer activity markers H3K4me1 and H3K27ac, which blocked the DNA binding of FOXO3, a critical mediator of the cellular response to oxidative stress, and suppressed antioxidative gene transcription. Moreover, KMT2D deletion in PCa cells also increased their sensitivity to genotoxic anticancer drugs and a PARP inhibitor, which suggested that lower levels of KMT2D may mediate the response of PCa to particular treatments. These findings further highlighted the important role of KMT2D in PCa progression and suggested that targeting KMT2D might be therapeutically beneficial for advanced PCa treatment.
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