Guest Editors
Prof. Xiao-Bin Lv, The third Affiliated Hospital of Nanchang University, the First Hospital of Nanchang, Nanchang, China.
Email: nclvxiaobin@sina.cn
Prof. Guoliang Huang, Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Guangdong Medical University, Guangzhou, China.
Email: huangguoliang@gdmu.edu.cn
Summary
Ferroptosis is a newly identified mode of programmed cell death characterized by an excess iron accumulation and subsequent unbalanced redox states. The molecular mechanism of ferroptosis is mainly dependent on the production and elimination of lipid peroxidation. When the peroxidation excess the capability which the cells could remove effectively through an antioxidative mechanism, the accumulation of peroxidative lipids induces ferroptosis. Many physiological processes including iron metabolism, amino acid metabolism, and lipid metabolism and a variety of gene-coding products including proteins, lncRNA, and miRNA, are implicated in ferroptosis.
Recently, growing studies have reported that chemotherapy, radiotherapy, and checkpoint therapy induce ferroptosis of cancer cell and the dysregulated ferroptosis could lead to the resistance of cancer to these therapies. Targeting ferroptosis-related signaling pathway could be new strategy for cancer therapy.
The objective of this Research Topic is to give a comprehensive overview of the regulatory mechanisms of ferroptosis and its potential applications in cancer treatment. We welcome Original Research, Reviews, Viewpoints etc., focusing on but not limited to the following topics:
1) Signaling pathways that regulate the cancer progression related to ferroptosis.
2) LncRNAs and miRNAs as the regulators of ferroptosis related to cancer.
3) Ferroptosis-related resistance or sensitivity to all kinds of cancer treatments.
Keywords
ferroptosis, cancer, peroxidative, iron
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