ArticlePeerJ2025
The BAF53A-BACH1-GCLM axis regulates glutathione metabolism and enhances ferroptosis resistance in esophageal squamous cell carcinoma.
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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5 authors.
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Abstract
Objective: Esophageal squamous cell carcinoma (ESCC), a highly lethal malignancy, exhibits poor survival rates and limited treatment options. Ferroptosis, a regulated form of cell death driven by lipid peroxidation, emerges as a potential therapeutic target. However, the mechanisms suppressing ferroptosis in ESCC remain poorly understood. Methods: Short hairpin RNA (shRNA) was employed to knock down BAF53A and BACH1 in ESCC cell lines, followed by assessments of cell proliferation, colony formation, and ferroptosis sensitivity. Glutathione (GSH) metabolism was evaluated by measuring GSH/GSSG and NADP Results: BAF53A was elevated in ESCC, and its depletion impaired cell proliferation and colony formation ability of cells. Knockdown of BAF53A disrupted GSH metabolism, leading to increased ROS levels, reduced GSH/GSSG and NADP Conclusions: The BAF53A-BACH1-GCLM axis constitutes a novel egulatory pathway that integrates chromatin remodeling, transcriptional regulatione, and ferroptosis resistance in ESCC. Targeting this axis may offer a promising approach to exploit metabolic vulnerabilities and enhance ferroptosis sensitivity in ESCC treatment.
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