ArticleCancer medicine2019
KMT2A histone methyltransferase contributes to colorectal cancer development by promoting cathepsin Z transcriptional activation.
Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 35 citations in OpenAlex.
- Cathepsin Z/X: Breaking Down the Known and Unknown.International journal of molecular sciences · 2026Review
- Gene expression and immune cell heterogeneity in inbred Amur tiger.BMC genomics · 2026Article
- Targeting Cathepsin Z suppresses endometriosis via the AMPK/mTOR-mediated autophagy and apoptosis axis.Frontiers in medicine · 2026Article
- KMT2A-Mediated transcriptional regulation in stemness and cancer: molecular mechanisms and therapeutic opportunities.Medical oncology (Northwood, London, England) · 2025Review
- Silencing KMT2A with siRNA induces apoptosis and cell cycle arrest in high-grade serous ovarian carcinoma cells by modulating GOF p53-dependent pathways, highlighting its potential as a therapeutic target.Medical oncology (Northwood, London, England) · 2025Article
- ATF2-mediated Transcriptional Activation of USP4 Stabilizes KMT2A Protein and Promotes Trophoblast Dysfunction.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Clinical and molecular results in 15 Turkish patients with Wiedemann-Steiner syndrome: identification of eight novel KMT2A variants and a case of dual molecular diagnosis in the CSNK2A1.European journal of pediatrics · 2025Article
- Are cathepsins a risk factor for papillary thyroid carcinoma? A bidirectional two-sample mendelian randomization analysis.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2025Article
- KMT2A degradation is observed in decitabine-responsive acute lymphoblastic leukemia cells.Molecular oncology · 2025Article
- KMT2A facilitates the epithelial-to-mesenchymal transition and the progression of ovarian cancer.Molecular and cellular biochemistry · 2025Article
- Prognostic and immunological implications of cathepsin Z overexpression in prostate cancer.Frontiers in immunology · 2025Article
- Evaluating the Relationship between Cathepsins and Papillary Thyroid Carcinoma: A Mendelian Randomization Study.Endocrine, metabolic & immune disorders drug targets · 2025Article
- Histone methyltransferase KMT2A: Developmental regulation to oncogenic transformation.The Journal of biological chemistry · 2024Review
- Unveiling the Molecular Landscape of Pancreatic Ductal Adenocarcinoma: Insights into the Role of the COMPASS-like Complex.International journal of molecular sciences · 2024Review
- Exploring Potential Epigenetic Biomarkers for Colorectal Cancer Metastasis.International journal of molecular sciences · 2024Review
- Article
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- The Role of Cysteine Protease Cathepsins B, H, C, and X/Z in Neurodegenerative Diseases and Cancer.International journal of molecular sciences · 2023Review
- Genomic landscape of locally advanced rectal adenocarcinoma: Comparison between before and after neoadjuvant chemoradiation and effects of genetic biomarkers on clinical outcomes and tumor response.Cancer medicine · 2023Article
- Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence supports the notion that epigenetic modifiers are abnormal in carcinogenesis and have a fundamental role in cancer progression. Among these aberrant epigenetic modifiers, the function of histone methyltransferase KMT2A in somatic tumors is not well known. By analyzing KMT2A expression in patient tissues, we demonstrated that KMT2A was overexpressed in colorectal cancer tissues in comparison with adjacent normal tissues and its expression was positively correlated with cancer stages. In KMT2A-knockdown HCT116 and DLD1 cells, cell invasion and migration were consequently suppressed. In addition, KMT2A depletion effectively suppressed cancer metastasis in vivo. Mechanistically, cathepsin Z (CTSZ) was demonstrated to be an important downstream gene of KMT2A. Further studies showed that p65 could recruit KMT2A on the promoter region of the downstream gene CTSZ and knockdown of p65 could reduce the KMT2A on the promoter of CTSZ. Finally, our present study revealed that KMT2A epigenetically promotes cancer progression by targeting CTSZ, which has specific functions in cancer invasion and metastasis.
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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.