ArticleCell death & disease2025
Transcription factor ONECUT3 regulates HDAC6/HIF-1α activity to promote the Warburg effect and tumor growth in colorectal cancer.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Periodontitis-Associated Circulating EVs Promote Colorectal Cancer Progression via Carnosine-Mediated Acidosis Adaptation.Cell proliferation · 2026Article
- Deciphering the tubulin code: roles and mechanisms of microtubule post-translational modifications in gastrointestinal tumors: a narrative review.Journal of gastrointestinal oncology · 2026Review
- Current research on the role of HIF in intervertebral disc degeneration.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Review
- Proton-Sensing G Protein-Coupled Receptors and Their Potential Role in Exercise Regulation of Arterial Function.Biomolecules · 2025Review
- Research progress on risk factors for in-stent restenosis following cerebrovascular stent implantation.Frontiers in neurology · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
The Warburg effect, also known as aerobic glycolysis, plays a crucial role in the onset and progression of colorectal cancer (CRC), although its mechanism remains unclear. In this study, bioinformatics analysis of public databases combined with validation using clinical specimens identified the transcription factor ONECUT3 as a key regulator related to the Warburg effect in CRC. Functionally, silencing ONECUT3 reverses the Warburg effect and suppresses tumor growth. Importantly, ONECUT3 promotes tumor growth in a glycolysis-dependent manner through hypoxia-inducible factor 1α (HIF-1α). Mechanistically, ONECUT3 does not directly regulate the expression of HIF-1α but instead inhibits its acetylation via histone deacetylase 6 (HDAC6). This deacetylation enhances the transcriptional activity of HIF-1α, ultimately upregulating multiple glycolysis-related genes downstream of HIF-1α, thereby driving the Warburg effect and facilitating tumor growth in CRC. These findings reveal a novel mechanism by which ONECUT3 regulates the Warburg effect in CRC and suggest that targeting ONECUT3 may offer a promising therapeutic strategy for CRC.
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