AI Article Synopsis
- Ferroptosis is a type of cell death driven by excess iron and lipid damage, influenced by abnormal enzyme activities.
- The regulatory mechanisms behind ferroptosis involve various levels of control, including changes in gene expression and epigenetic modifications, like N-methyladenosine (mA).
- Research indicates that altered ferroptosis linked to mA may promote tumor growth, highlighting its potential as a target for cancer diagnosis and treatment strategies.
Article Abstract
Ferroptosis is an iron-dependent regulatory cell necrosis induced by iron overload and lipid peroxidation. It occurs when multiple redox-active enzymes are ectopically expressed or show abnormal function. Hence, the precise regulation of ferroptosis-related molecules is mediated across multiple levels, including transcriptional, posttranscriptional, translational, and epigenetic levels. N-methyladenosine (mA) is a highly evolutionarily conserved epigenetic modification in mammals. The mA modification is commonly linked to tumor proliferation, progression, and therapy resistance because it is involved in RNA metabolic processes. Intriguingly, accumulating evidence suggests that dysregulated ferroptosis caused by the mA modification drives tumor development. In this review, we summarized the roles of mA regulators in ferroptosis-mediated malignant tumor progression and outlined the mA regulatory mechanism involved in ferroptosis pathways. We also analyzed the potential value and application strategies of targeting mA/ferroptosis pathway in the clinical diagnosis and therapy of tumors.
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| http://dx.doi.org/10.1007/s11427-023-2474-4 | DOI Listing |
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