文献类型：期刊文献

英文题名：Zinc Finger Protein 263 Augments Autophagy and Promotes Intrahepatic Cholangiocarcinoma Proliferation

作者：Yan, Zaihua[1];Du, Yadan[2];Chen, Yawen[2];Yang, Jian[3];Zhang, Haoyang[1];Da, Mingxu[1,3]

第一作者：Yan, Zaihua

通信作者：Da, M[1];Da, M[2]

机构：[1]Lanzhou Univ, Sch Clin Med 1, Lanzhou, Peoples R China;[2]Gansu Univ Chinese Med, Lanzhou, Peoples R China;[3]Gansu Prov Hosp, Dept Surg Oncol, Lanzhou, Peoples R China

第一机构：Lanzhou Univ, Sch Clin Med 1, Lanzhou, Peoples R China

通信机构：[1]corresponding author), Lanzhou Univ, Sch Clin Med 1, Lanzhou, Peoples R China;[2]corresponding author), Gansu Prov Hosp, Dept Surg Oncol, Lanzhou, Peoples R China.

年份：2024

外文期刊名：MOLECULAR CARCINOGENESIS

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001356846300001)】；

基金：We thank Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences for providing us with conditions of animal experiments. We thank Shanghai Outdo Biotech Company for providing the construction of the intrahepatic cholangiocarcinoma tissue chip. In addition, we are grateful to OE Biotech Co. Ltd. (Shanghai, China) for its technical support regarding the RNA-seq and CUT&Tag. This work was supported by the National Natural Science Foundation of China (No: 82160588), the Gansu Natural Science Foundation (No: 21JR1RA016, No: 21JR7RA598), and the Gansu Youth Natural Science Foundation (No: 21JR7RA645, No: 21JR7RA646).

语种：英文

外文关键词：autophagy; intrahepatic cholangiocarcinoma; proliferation; ULK1; ZNF263

摘要：Intrahepatic cholangiocarcinoma (ICC) is an aggressive cancer characterized by a poor prognosis. Despite Zinc finger proteins (ZNFs) importance in tumor development and progression, it is unknown how dysregulated ZNF263 contributes to intrahepatic cholangiocarcinoma. 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&Tag, RNA-seq, CHIP-PCR, 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-expressing ameliorated ZNF263 knockdown-induced inhibition of CRC proliferation. By activating the ULK1-autophagy axis, ZNF263 promotes proliferation of ICC and is potentially a prognostic or therapeutic target of ICC.