ArticleJournal of cancer research and clinical oncology2022
Histone methyltransferase KMT2C plays an oncogenic role in prostate cancer.
Article in Journal of cancer research and clinical oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- Molecular Biomarkers of Glioma.Biomedicines · 2025Review
- Mutations in epigenetic regulatorOncology research · 2023Article
- Comprehensive germline and somatic genomic profiles of Chinese patients with biliary tract cancer.Frontiers in oncology · 2022Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
purposeProstate cancer (PCa) is a leading cause of morbidity and mortality in males. Epigenetic modifier abnormalities are becoming a driving event in PCa. The specific role of KMT2C, a histone methyltransferase that is frequently aberrant in various tumors, is poorly understood in PCa. This study aimed to reveal the potential carcinogenic role of KMT2C in PCa.
methodsWe first examined the expression levels of KMT2C in prostate cancer tissues. Then, we assessed the function of KMT2C in prostate cancer cell proliferation, colony formation, and migration. To explore the mechanism of the biological consequences, RNA-seq and CHIP-qPCR were performed. We also analyzed the effects of overexpression of the KMT2C downstream genes CLDN8 and ITGAV to reverse the effects of KMT2C on prostate cancer cells.
resultsHerein, we first confirmed KMT2C overexpression in PCa at the transcript and protein levels. Knocking down KMT2C in VCaP and LNCaP cells inhibited cell viability, colony formation, and migration. Consistently, stable KMT2C depletion effectively decreased tumor growth by approximately 70% in vivo. Mechanistically, the results suggested that CLDN8 and ITGAV are two key downstream genes of KMT2C and further regulate the MAPK/ERK and EMT pathways.
conclusionOur study suggests that KMT2C plays an oncogenic role in PCa. One of the mechanisms may be the epigenetic regulation of CLDN8 and ITGAV by KMT2C to modulate tumor-signaling pathways. Therefore, KMT2C may serve as a potential therapeutic target for PCa patients.
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