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Regulation of Ferroptosis in Lung Adenocarcinoma

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MDPI
DOI: 10.3390/ijms241914614

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ferroptosis; regulation; lung adenocarcinoma; therapy

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Lung adenocarcinoma (LUAD) is the most common type of lung cancer, and there is a need to explore novel targets and drugs to improve outcomes. Ferroptosis, an iron-dependent regulated cell death, has gained attention as a potential therapeutic target for LUAD. This review provides an overview of the mechanisms and regulation of ferroptosis in LUAD, as well as its application in therapy.
Lung adenocarcinoma (LUAD) is the most common lung cancer, which accounts for about 35-40% of all lung cancer patients. Despite therapeutic advancements in recent years, the overall survival time of LUAD patients still remains poor, especially KRAS mutant LUAD. Therefore, it is necessary to further explore novel targets and drugs to improve the prognos is for LUAD. Ferroptosis, an iron-dependent regulated cell death (RCD) caused by lipid peroxidation, has attracted much attention recently as an alternative target for apoptosis in LUAD therapy. Ferroptosis has been found to be closely related to LUAD at every stage, including initiation, proliferation, and progression. In this review, we will provide a comprehensive overview of ferroptosis mechanisms, its regulation in LUAD, and the application of targeting ferroptosis for LUAD therapy.

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