ArticleMolecular cancer2022
KMT2C methyltransferase domain regulated INK4A expression suppresses prostate cancer metastasis.
Article in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 50 citations in OpenAlex.
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- Biobank of genetically defined murine prostate cancer tumoroids uncovers oncogenic pathways and drug vulnerabilities driven by PTEN-loss.Cell reports methods · 2026Article
- KMT2C Loss Promotes NF2-Wildtype Meningioma Progression and Ferroptosis Sensitivity via Epigenetic Repression of Hippo Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Curcumin: biochemistry, pharmacology, advanced drug delivery systems, and its epigenetic role in combating cancer.Frontiers in pharmacology · 2025Review
- Insights into the mechanisms driven by H3K4 KMTs in pancreatic cancer.The Biochemical journal · 2024Review
- Enzalutamide inhibits PEX10 function and sensitizes prostate cancer cells to ROS activators.Cell death & disease · 2024Article
- A pan-cancer interrogation of intronic polyadenylation and its association with cancer characteristics.Briefings in bioinformatics · 2024Article
- JUN mediates the senescence associated secretory phenotype and immune cell recruitment to prevent prostate cancer progression.Molecular cancer · 2024Article
- CRISPR/Cas9 model of prostate cancer identifies Kmt2c deficiency as a metastatic driver by Odam/Cabs1 gene cluster expression.Nature communications · 2024Article
- Heparanase inhibitor OGT 2115 induces prostate cancer cell apoptosis via the downregulation of MCL‑1.Oncology letters · 2024Article
- The modification role and tumor association with a methyltransferase: KMT2C.Frontiers in immunology · 2024Review
- Evolutionary signatures of human cancers revealed via genomic analysis of over 35,000 patients.Nature communications · 2023Article
- Pre-Clinical Models to Study Human Prostate Cancer.Cancers · 2023Review
- Addressing the Reciprocal Crosstalk between the AR and the PI3K/AKT/mTOR Signaling Pathways for Prostate Cancer Treatment.International journal of molecular sciences · 2023Review
- Mutations in epigenetic regulatorOncology research · 2023Article
- An anoikis-related gene signature for prediction of the prognosis in prostate cancer.Frontiers in oncology · 2023Article
- Comprehensive germline and somatic genomic profiles of Chinese patients with biliary tract cancer.Frontiers in oncology · 2022Article
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Authors and funding
24 authors at 7 institutions in 3 countries.
Funding
Abstract
backgroundFrequent truncation mutations of the histone lysine N-methyltransferase KMT2C have been detected by whole exome sequencing studies in various cancers, including malignancies of the prostate. However, the biological consequences of these alterations in prostate cancer have not yet been elucidated.
methodsTo investigate the functional effects of these mutations, we deleted the C-terminal catalytic core motif of Kmt2c specifically in mouse prostate epithelium. We analysed the effect of Kmt2c SET domain deletion in a Pten-deficient PCa mouse model in vivo and of truncation mutations of KMT2C in a large number of prostate cancer patients.
resultsWe show here for the first time that impaired KMT2C methyltransferase activity drives proliferation and PIN formation and, when combined with loss of the tumour suppressor PTEN, triggers loss of senescence, metastatic dissemination and dramatically reduces life expectancy. In Kmt2c-mutated tumours we show enrichment of proliferative MYC gene signatures and loss of expression of the cell cycle repressor p16
conclusionsWe identified truncating events of KMT2C as drivers of proliferation and PIN formation. Loss of PTEN and KMT2C in prostate cancer results in loss of senescence, metastatic dissemination and reduced life expectancy. Our data demonstrate the prognostic significance of KMT2C mutation status in prostate cancer patients. Inhibition of the MYC signalling axis may be a viable treatment option for patients with KMT2C truncations and therefore poor prognosis.
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