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This study aimed to determine whether ZNF263 plays an oncogenic role in ICC progression. The microarray of tumor tissues from clinical intrahepatic cholangiocarcinoma was immunohistochemically analyzed for ZNF263. Based on plate colony formation, CCK8, and tumor xenograft models, ZNF263 was assessed for its biological function. Mechanistically, CUT&amp;Tag, RNA\u2010seq, CHIP\u2010PCR, Dual luciferase reporter assay, Western blotting, transmission electron microscopy (TEM), and immunohistochemical staining were employed. ZNF263 expression was elevated in intrahepatic cholangiocarcinoma tissues compared to nontumor tissues, which negatively impacted patient outcomes. Notably, ZNF263 overexpression promoted ICC cells proliferation via enhancing autophagy, whereas ZNF263 knockdown inhibited ICC cells proliferation. Furthermore, ZNF263 binds to the enhancer region of ULK1 and mediates its expression. ULK1 over\u2010expressing ameliorated ZNF263 knockdown\u2010induced inhibition of CRC proliferation. By activating the ULK1\u2010autophagy axis, ZNF263 promotes proliferation of ICC and is potentially a prognostic or therapeutic target of ICC.<\/jats:p>","DOI":"10.1002\/mc.23847","type":"journal-article","created":{"date-parts":[[2024,11,18]],"date-time":"2024-11-18T12:23:42Z","timestamp":1731932622000},"page":"317-328","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Zinc Finger Protein 263 Augments Autophagy and Promotes Intrahepatic Cholangiocarcinoma Proliferation"],"prefix":"10.1002","volume":"64","author":[{"given":"Zaihua","family":"Yan","sequence":"first","affiliation":[{"name":"The First School of Clinical Medicine Lanzhou University Lanzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yadan","family":"Du","sequence":"additional","affiliation":[{"name":"Gansu University of Chinese Medicine Lanzhou 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