ArticleCell death & disease2025
TACC3 enhances glycolysis in bladder cancer cells through inducing acetylation of c-Myc.
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 9 papers.
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Who cites it
9 citing papers in PubMed.
- ATAD3A promotes bladder cancer progression by regulating glycolysis through MYC stabilization.Journal of translational medicine · 2026Article
- Gene Polymorphisms Associated with Osteoarthritis: Potential Implications for Nutrigenetics and Precision Nutrition.Nutrients · 2026Review
- HMGB1-mediated enhancement of glycolysis activates hepatic stellate cells by inhibiting ferroptosis in alcoholic hepatic fibrosis.Stem cell research & therapy · 2026Article
- Post-translational modifications: Principal regulators of bladder cancer.Molecular biology reports · 2026Review
- Targeting Glycolytic Metabolism in Cancer Therapy: Current Approaches and Future Perspectives.Cells · 2026Review
- The GFPT2/O-GlcNAcylation/c-Myc axis promotes bladder cancer progression.Journal of translational medicine · 2026Article
- Mechanical stress, metabolic reprogramming and stromal remodeling: an emerging paradigm in the bladder cancer mechano-micro-environment.Frontiers in genetics · 2026Review
- Regulation of drug resistance in bladder urothelial carcinoma by tumor aerobic glycolysis.Journal of translational medicine · 2025Review
- HOXA9 drives lymphatic metastasis by activating the c-MYC-glycolysis-lactate axis in gastric cancer.Journal of translational medicine · 2025Article
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Authors and funding
6 authors.
Funding
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Abstract
The proliferation of bladder cancer (BC) cells is driven by metabolic reprogramming, marked by a glycolytic dependency to sustain uncontrolled growth. While Transforming Acidic Coiled-Coil Containing Protein 3 (TACC3) is known to promote BC progression and correlate with poor prognosis, the mechanisms underlying its upregulation and role in aerobic glycolysis remain unclear. Here, we identify E2F3 as a direct transcriptional activator of TACC3, with its amplification in BC driving elevated TACC3 expression. TACC3 overexpression enhances glycolysis, increasing glucose consumption, lactate production, and expression of glycolytic enzymes (e.g., GLUT1, HK2, PFKFB3), while its knockdown suppresses these effects. Pharmacological inhibition of glycolysis abrogates TACC3-driven tumor growth in vitro and in vivo. Mechanistically, TACC3 interacts with c-Myc, promoting its acetylation at lysine 323 (K323) by recruiting the acetyltransferase PCAF and antagonizing the deacetylase SIRT1. This acetylation stabilizes c-Myc, amplifying its transcriptional activation of glycolytic targets. Our findings establish TACC3 as a critical regulator of c-Myc-driven metabolic reprogramming in BC, highlighting its potential as a therapeutic target to disrupt glycolysis and oncogenic c-Myc signaling.
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