ArticleJournal of experimental & clinical cancer research : CR2025
CDCA3-MYC positive feedback loop promotes bladder cancer progression via ENO1-mediated glycolysis.
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Identification of MYC co-expression gene: POLR3G is associated with cell senescence, immunotherapy, chemotherapy responses, and clinical prognosis in bladder cancer patients.Translational oncology · 2026Article
- FBXL6 promotes bladder cancer progression by stabilizing ENO1 through K63-linked ubiquitination.Cell death discovery · 2026Article
- TRIM28 orchestrates SUMO-ubiquitin crosstalk to stabilize PPARG and drive bladder cancer progression.Cell death & disease · 2026Article
- Aerobic glycolysis in bladder cancer: research advances and targeted therapy potential.Frontiers in oncology · 2026Review
- CEACAM6 regulates glycolytic metabolism in bladder cancer cell by controlling ENO1 stability.European journal of medical research · 2025Article
- KBTBD11 suppresses hepatocellular carcinoma by targeting ENO1-mediated glycolysis.Journal of translational medicine · 2025Article
- The functional roles of deoxyelephantopin potential target circTNPO3 in regulating pancreatic cancer malignant phenotype and gemcitabine chemoresistance via miR-188-5p/CDCA3/TRAF2-mediated remodeling of NF-κB signaling pathway.Frontiers in pharmacology · 2025Article
- Macrophages: emerging targets for ulcerative colitis.Frontiers in immunology · 2025Review
- ULK2 suppresses glycolysis to attenuate cisplatin resistance in ovarian cancer organoid via c-Jun phosphorylation.Science progressArticle
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundBladder cancer (BLCA) ranks among the most prevalent malignancies of the urinary system, with its clinical diagnosis predominantly reliant on invasive procedures. Traditional chemotherapy regimens exhibit significant limitations, underscoring the urgency of identifying novel diagnostic biomarkers and strategies to enhance chemotherapy efficacy. CDCA3 has been recognized as a facilitator of BLCA progression, activated by MYBL2. However, its precise regulatory mechanisms in BLCA pathogenesis remain incompletely elucidated.
methodsTo investigate the functional role of CDCA3 in BLCA, MTT and colony formation assays were employed to assess cellular proliferation, while flow cytometry was utilized to evaluate apoptosis and intracellular ROS levels. The expression of CDCA3, ENO1, TRIM28, and MYC was analyzed through WB and qRT-PCR, and Co-IP assays were conducted to delineate interactions among CDCA3, TRIM28, and MYC.
resultsCDCA3, a key regulator of the cell cycle, facilitates BLCA glycolysis by modulating the transcriptional expression of α-Enolase (ENO1), thereby enhancing BLCA progression. Mechanistically, CDCA3 recruits TRIM28, which stabilizes MYC, while MYC transcriptionally upregulates CDCA3, establishing a self-reinforcing CDCA3-MYC feedback loop. A risk prediction model incorporating the expression profiles of CDCA3 and ENO1 was developed to evaluate the overall survival of patients with BLCA. This model provides a prognostic tool to predict survival outcomes in patients with BLCA based on CDCA3 and ENO1 expression levels.
conclusionsThis study delineates a novel role for CDCA3 in the regulation of BLCA glycolysis and identifies its interaction with MYC as a critical positive feedback mechanism, providing fresh insights into the molecular mechanisms underlying BLCA progression.
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