ArticleCell & bioscience2022
Histone methyltransferase KMT2D cooperates with MEF2A to promote the stem-like properties of oral squamous cell carcinoma.
Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Experimental Models and Nanotechnology-Based Platforms in Oral Squamous Cell Carcinoma: From Tumor Biology to Translational Applications.Pharmaceutics · 2026Review
- Review
- Advancing oral squamous cell carcinoma research: the evolving role of patient-derived cell lines, xenografts, and organoid models.3 Biotech · 2025Review
- Evolving role of deubiquitinating enzymes in oral cancer (Review).Oncology letters · 2025Review
- Targeting Epigenetic Dysregulations in Head and Neck Squamous Cell Carcinoma.Journal of dental research · 2025Review
- Molecular insight into histone methylation as a novel target for oral squamous cell carcinoma: future hope in personalised medicine.Journal of Cancer · 2025Review
- Histone-methyltransferase KMT2D deficiency impairs the Fanconi anemia/BRCA pathway upon glycolytic inhibition in squamous cell carcinoma.Nature communications · 2024Article
- Knockdown of Kmt2d leads to growth impairment by activating the Akt/β-catenin signaling pathway.G3 (Bethesda, Md.) · 2024Article
- Exploring Potential Epigenetic Biomarkers for Colorectal Cancer Metastasis.International journal of molecular sciences · 2024Review
- The repertoire of mutational signatures in tobacco- and non-tobacco-induced oral cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Oral squamous cell carcinomas: state of the field and emerging directions.International journal of oral science · 2023Review
- Histone modifications in drug-resistant cancers: From a cancer stem cell and immune evasion perspective.Experimental & molecular medicine · 2023Review
- The expression and methylation ofFrontiers in genetics · 2022Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEpigenetic reprogramming is involved in multiple steps of human cancer evolution and is mediated by a variety of chromatin-modifying enzymes. Specifically, the histone lysine methyltransferase KMT2D is among the most frequently mutated genes in oral squamous cell carcinoma (OSCC). However, the mechanisms by which KMT2D affects the development of OSCC remain unclear.
resultsIn the present study, we found that the expression of KMT2D was elevated in OSCC compared to paracancerous specimens and was correlated with a more advanced tumor grade. More importantly, knockdown of KMT2D impaired their reconstitution in patient-derived organoids and decreased the expression of CD133 and β-catenin in OSCC cells. In in vitro and in vivo models, knockdown of KMT2D reduced the colony formation, migration and invasion abilities of OSCC cells and delayed tumor growth. Mechanistically, the dual-luciferase reporter and co-immunoprecipitation assays in two individual OSCC cell lines indicated that KMT2D may cooperate with MEF2A to promote the transcription activity of CTNNB1, thereby enhancing WNT signaling.
conclusionThe upregulation of KMT2D contributes to stem-like properties in OSCC cells by sustaining the MEF2A-mediated transcriptional activity of CTNNB1.
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