4.7 Review

Ferroptosis as a novel form of regulated cell death: Implications in the pathogenesis, oncometabolism and treatment of human cancer

Journal

GENES & DISEASES
Volume 9, Issue 2, Pages 347-357

Publisher

ELSEVIER
DOI: 10.1016/j.gendis.2020.11.019

Keywords

Cancer; Cancer therapy; Clinical application; Ferroptosis; Lipid peroxidation; Pathogenesis

Funding

  1. National Natural Science Foundation of China [81904231,82072978,82072979]
  2. China Postdoctoral Science Foundation [2020M672369]
  3. Natural Science Foundation of Hubei Province [2020CFB861]
  4. Postdoctoral Innovation Practice Post in Hubei Province [34]

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The treatment of cancer involves surgical excision, radiotherapy, and chemotherapy. Chemotherapy drugs interfere with tumor growth and induce cancer cell death. Ferroptosis, a newly discovered iron-dependent type of cell death, is negatively correlated with cancer development and primarily caused by an abnormal increase in iron-dependent reactive oxygen species and the imbalance of redox homeostasis.
The treatment of cancer mainly involves surgical excision supplemented by radiotherapy and chemotherapy. Chemotherapy drugs act by interfering with tumor growth and inducing the death of cancer cells. Anti-tumor drugs were developed to induce apoptosis, but some patient's show apoptosis escape and chemotherapy resistance. Therefore, other forms of cell death that can overcome the resistance of tumor cells are important in the context of cancer treatment. Ferroptosis is a newly discovered iron-dependent, non-apoptotic type of cell death that is highly negatively correlated with cancer development. Ferroptosis is mainly caused by the abnormal increase in iron-dependent lipid reactive oxygen species and the imbalance of redox homeostasis. This review summarizes the progression and regulatory mechanism of ferroptosis in cancer and discusses its possible clinical applications in cancer diagnosis and treatment. Copyright (C) 2020, Chongqing Medical University. Production and hosting by Elsevier B.V.

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