TACC3 enhances glycolysis in bladder cancer cells through inducing acetylation of c-Myc.

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 vi

SUBMITTER: Lin Z 

PROVIDER: S-EPMC12006502 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature