ArticleIn vitro cellular & developmental biology. Animal2026
ALKBH4 confers ferroptosis resistance and drives tumorigenesis via dysregulation of GPX4 in breast cancer cells.
Article in In vitro cellular & developmental biology. Animal, 2026. 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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Abstract
Breast cancer (BC) remains a predominant source of cancer-related fatalities among women globally. While the AlkB homolog family member ALKBH4 has been implicated in cancer, its role and mechanism in BC are unknown. Its role within BC and its correlation with ferroptosis-a type of iron-mediated regulated cell death, were examined in this work. Data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and immunohistochemistry (IHC) analyses indicate ALKBH4 overexpression in BC, further associating its high expression levels with unfavorable clinical outcomes. Functional experiments in BC cells demonstrated that ALKBH4 knockdown exerted inhibitory effects on proliferation, migration, and invasion. Concurrently, it promoted apoptosis. Transcriptomic and biochemical investigations revealed that knocking down ALKBH4 sets off a ferroptotic cascade, with telltale signs including heightened levels of malondialdehyde (MDA) and ferrous iron (Fe
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