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Identifying the factors driving GBC progression is crucial for developing potent preventive and therapeutic approaches. Here, using quantitative proteomics, we identify GALNT7 as the most significantly upregulated glycosyltransferase in GBC tissues, associated with adverse clinical outcomes. Mechanistically, GALNT7 physically interacts with TAZ and catalyzes O\u2010GalNAcylation at Ser307, thereby inhibiting K48\u2010linked ubiquitination through the recruitment of the deubiquitinase USP7 and stabilizing the TAZ protein. This post\u2010translational modification promotes TAZ accumulation and subsequent activation of TEAD1\u2010mediated transcription, which in turn upregulates GALNT7 expression, thereby establishing a self\u2010reinforcing oncogenic feedback loop. Disruption of TAZ O\u2010GalNAcylation via the S307A mutation abrogates its oncogenic activity and attenuates GALNT7\u2010driven tumor progression. Importantly, structure\u2010based drug\u2010repurposing screens identified the PARP inhibitor Olaparib as a direct GALNT7 antagonist that effectively inhibits TAZ O\u2010GalNAcylation and demonstrates potent anti\u2010tumor efficacy against GBC both in vitro and in vivo. Collectively, our findings reveal a glycosylation\u2010dependent regulatory axis that drives GBC progression and establish GALNT7\u2010TAZ signaling as a tractable therapeutic target.<\/jats:p>","DOI":"10.1002\/advs.76490","type":"journal-article","created":{"date-parts":[[2026,7,11]],"date-time":"2026-07-11T18:33:26Z","timestamp":1783794806000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Targeting GALNT7 Disrupts the TAZ O\u2010GalNAcylation Feedback Loop to Suppress Gallbladder Cancer Progression"],"prefix":"10.1002","volume":"13","author":[{"given":"Peng","family":"Qiu","sequence":"first","affiliation":[{"name":"Division of Hepato\u2010Pancreato\u2010Biliary Surgery Tongji Hospital Tongji Medical College Huazhong University of Science &amp; Technology  Wuhan Hubei P. R. China"},{"name":"Hubei Key Laboratory of Hepato\u2010Pancreato\u2010Biliary Diseases  Wuhan Hubei P. R. 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