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MINI REVIEW article
Front. Oncol.
Sec. Molecular and Cellular Oncology
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1573378
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Autophagy-related genes (ATGs) play a crucial role in tumorigenesis and cancer progression. ATG10, a member of the ATG family, has been implicated in various malignancies, including endometrial cancer, hepatocellular carcinoma, acute leukaemia, nasopharyngeal carcinoma, gastric cancer and colorectal cancer. Its overexpression is frequently associated with poor prognosis and increased disease progression. ATG10 promotes cancer growth and metastasis by modulating epithelial-mesenchymal transition and cell cycle regulators such as cyclin B1, CDK1 and CDK2. However, its activity can be inhibited by several factors, including DDX10, PTBP1, sodium orthovanadate, podofilox, SIRT6, FAT1, SOX2 and multiple microRNAs (e.g., miR-369-3p, miR-100-3p, miR-27b-3p, miR-197-3p, let-7i-5p and miR-552). This review explores the functional and clinical significance of ATG10 across various cancers, highlighting its potential as a biomarker and therapeutic target.
Keywords: ATG10, Epithelial-Mesenchymal Transition, Cancer, review, Therapeutic target
Received: 08 Feb 2025; Accepted: 27 Mar 2025.
Copyright: © 2025 Shi, Ke, Li, Shi, Liu, Li and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Dan Li, Taihe Hospital, Hubei University of Medicine, Shiyan, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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