ArticlePloS one2025
6-Methoxyflavone targets SLC1A5 to induce ferroptosis in HeLa cells.
Article in PloS one, 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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Abstract
objectiveThis study aimed to explore the role and molecular mechanism of 6-methoxyflavone in inducing ferroptosis in HeLa cells.
methodsTransmission electron microscopy (TEM), mitochondrial superoxide, and glutathione content assay were used to detect the effects of 6-methoxyflavone on ferroptosis. Tandem mass tag and parallel reaction monitoring proteomics, non-targeted and targeted metabolomics, polymerase chain reaction (qPCR), western blot, alternative splicing, new transcript, functional domain, molecular docking, non-covalent interaction, loss-of-function genetic manipulation, and mitochondrial superoxide analyses were performed to explore the molecular mechanism of 6-methoxyflavone-induced ferroptosis in HeLa cells.
results6-Methoxyflavone induced ferroptosis in HeLa cells. Multi-omics, qPCR, western blot, alternative splicing, new transcript, functional domain, molecular docking, non-covalent interaction, loss-of-function genetic manipulation, and mitochondrial superoxide analyses indicated that 6-methoxyflavone induced ferroptosis in HeLa cells by upregulating the expression levels of SLC1A5 and mitochondrial superoxide. Molecular docking analyses showed that 6-methoxyflavone had the strongest affinity for SLC1A5. Non-covalent interaction analyses suggested that the interaction between 6-methoxyflavone and SLC1A5 was primarily driven by hydrophobic interactions. 6-Methoxyflavone targeted the peptide segment sequence LGPEGELLIR of SLC1A5.
conclusion6-Methoxyflavone induced ferroptosis in HeLa cells by markedly altering ferroptosis-related genes, proteins, and metabolites expression, thereby exerting anti-cancer effects. The core gene responsible for the induction of ferroptosis and the upregulation of mitochondrial superoxide in HeLa cells by 6-methoxyflavone is SLC1A5.
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