ArticleDiscover oncology2025
ATG7-induced autophagy inhibits ferroptosis and promotes the progression of colorectal adenocarcinoma.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Autophagy Dysregulation in Crohn's Disease and Colorectal Cancer-An Analysis ofCurrent issues in molecular biology · 2025Article
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4 authors.
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Abstract
purposeTo investigate the role of ATG7-induced autophagy in regulating ferroptosis and promoting the progression of colorectal adenocarcinoma (COAD).
methodThe UALCAN database was used to predict the expression of ATG7 and its prognosis significance in patients with COAD. The expression levels of ATG7 in HCT8 and SW620 cells were analyzed using qPCR and Western blot analyses. Functional assays, including the CCK-8 and Transwell assays, were conducted to assess the effects of ATG7 overexpression on cell proliferation and migration. Protein-protein interaction analyses were performed using GeneMANIA and STRING to explore the relationships between ATG7, autophagy-related proteins, and markers of ferroptosis. Autophagy was inhibited using 3-MA, while ferroptosis was induced with erastin in ATG7-overexpressing COAD cells to elucidate their interactions.
resultsOverexpression of ATG7 in COAD cells enhanced cell proliferation and migration, while inhibiting ferroptosis by decreasing levels of Fe
conclusionThese findings suggest that targeting ATG7-mediated autophagy may serve as a therapeutic strategy for COAD by increasing susceptibility to ferroptosis-induced cell death.
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