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Integrative analyses across multiple HCC cohorts identified TUBA1B as one of the most consistently upregulated tubulin isotypes whose high expression associates with poor prognosis and metastasis. In hydrodynamic tail\u2010vein injection (HTVi) models, co\u2010expression of\n                    <jats:italic>Tuba1b<\/jats:italic>\n                    with\n                    <jats:italic>myr\u2010AKT<\/jats:italic>\n                    enhanced liver tumor growth, supporting a tumor\u2010promoting role for\n                    <jats:italic>Tuba1b<\/jats:italic>\n                    in vivo. TUBA1B knockdown suppressed HCC cell proliferation, migration, and invasion in vitro and reduced tumor growth and metastasis in orthotopic models. HTVi\u2010mediated delivery of sg\n                    <jats:italic>Tuba1b<\/jats:italic>\n                    suppressed hepatocarcinogenesis in\n                    <jats:italic>NRasV12\/myr\u2010AKT<\/jats:italic>\n                    \u2013 and\n                    <jats:italic>MYC\/sg\u2010p53<\/jats:italic>\n                    HCC models and prolonged survival in the former, whereas sg\n                    <jats:italic>Tuba1b<\/jats:italic>\n                    delivery to normal livers caused no detectable histological abnormalities. Mechanistically, TUBA1B bound and stabilized G3BP2 by restraining TRIM25\u2010dependent K48\u2010linked ubiquitination, thereby promoting G3BP2\u2013I\u03baB\u03b1 association and sustaining basal NF\u2010\u03baB\/p65 transcriptional activity; enforced G3BP2 expression rescued the proliferative and metastatic defects caused by TUBA1B loss. Clinically, combined upregulation of TUBA1B and G3BP2 with elevated p65 activity delineated a high\u2010risk HCC subgroup with the poorest outcomes. Collectively, these findings define a TUBA1B\u2013G3BP2 stability axis that supports malignant phenotypes and highlight a potential therapeutic vulnerability in HCC.\n                  <\/jats:p>","DOI":"10.1002\/advs.77502","type":"journal-article","created":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T05:11:51Z","timestamp":1788757911000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["The TUBA1B\u2013G3BP2 Axis Sustains p65 Transcriptional Activity to Promote Hepatocellular Carcinoma Progression"],"prefix":"10.1002","author":[{"given":"Fen","family":"Lin","sequence":"first","affiliation":[{"name":"State Key Laboratory of Systems Medicine for Cancer Shanghai Cancer Institute Renji Hospital Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hechun","family":"Lin","sequence":"additional","affiliation":[{"name":"State Key Laboratory 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