ArticleEuropean journal of medical research2024
Inactivation of KDM6A promotes the progression of colorectal cancer by enhancing the glycolysis.
Article in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed.
- CHIP/STUB1 suppresses colorectal tumorigenesis through ubiquitin-mediated degradation of LDHA and inhibition of glycolysis.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Whole exome sequencing identifies somatically mutated genes in bladder cancer: A pilot study from Bangladesh.Biochemistry and biophysics reports · 2026Article
- Glucose Metabolism Regulating Colorectal Cancer Initiation and Progression.Cancer science · 2026Review
- The tumor immune microenvironment of thyroid cancer and colorectal cancer: cellular crosstalk and therapeutic implications.Frontiers in immunology · 2026Review
- The Identification by Shotgun Proteomics with High-Resolution Tandem Mass-Spectrometry of Histone Isoforms' Hypermethylation Phenotype as a Hallmark Characteristic of Human-IDH-Mutant High-Grade Gliomas: Epigenetic Applications for Genotoxicity-Based Biomarkers and Cancer Therapy Targets.Journal of proteome research · 2025Article
- Review
- Gender and sex interactions are intrinsic components of cancer phenotypes.Nature reviews. Cancer · 2025Review
- Demystifying the Role of Histone Demethylases in Colorectal Cancer: Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2025Review
- Role of glucose metabolic reprogramming in colorectal cancer progression and drug resistance.Translational oncology · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
KDM6A (lysine demethylase 6A) has been reported to undergo inactivating mutations in colorectal cancer, but its function in the progression of colorectal cancer has not been evaluated using animal models of colorectal cancer. In this study, we found that knocking out KDM6A expression in mouse intestinal epithelium increased the length of villus and crypt, promoting the development of AOM (azoxymethane)/DSS (dextran sulfate sodium salt)-induced colorectal cancer. On the other hand, knocking down KDM6A expression promoted the growth of colorectal cancer cells. In molecular mechanism studies, we found that KDM6A interacts with HIF-1α; knocking down KDM6A promotes the binding of HIF-1α to the LDHA promoter, thereby promoting LDHA expression and lactate production, enhancing glycolysis. Knocking down LDHA reversed the malignant phenotype caused by KDM6A expression loss. In summary, this study using animal models revealed that KDM6A loss promotes the progression of colorectal cancer through reprogramming the metabolism of the colorectal cancer cells, suggesting that restoring the function of KDM6A is likely to be one of the strategies for colorectal cancer treatment.
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Registered trials
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.