A review shows that ATG10 has been identified as a potential prognostic marker and therapeutic target for cancer patients based on real-world studies

TL;DR

This review highlights how ATG10 contributes to cancer progression and could help predict outcomes or guide treatments for cancer patients.

Contribution

The paper systematically reviews ATG10's role in multiple cancers and its potential as a prognostic marker and therapeutic target.

Findings

ATG10 overexpression is linked to poor prognosis and cancer progression in several malignancies.

ATG10 promotes cancer growth by affecting cell cycle regulators and epithelial-mesenchymal transition.

Multiple factors and microRNAs can inhibit ATG10 activity, offering potential therapeutic strategies.

Abstract

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 leukemia, 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.

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