Emerging mechanisms and targeted therapy of ferroptosis in cancer.

Apr 5, 2021

Contributor: Haiyan Wang,Yan Cheng,Chao Mao,Shuang Liu,Desheng Xiao,Jun Huang,Yongguang Tao

Emerging mechanisms and targeted therapy of ferroptosis in cancer.

Ferroptosis is an iron- and lipid ROS-dependent form of programmed cell death that is distinct from other forms of regulatory cell death at the morphological, biological and genetic levels. Emerging evidence suggests critical roles for ferroptosis in cell metabolism, the redox status and various diseases, such as cancers, nervous system diseases, and ischemia-reperfusion injury, with ferroptosis-related proteins. Ferroptosis is inhibited in diverse cancer types and functions as a dynamic tumor suppressor in cancer development, indicating that the regulation of ferroptosis can be utilized as an interventional target for tumor treatment. Small molecules and nanomaterials that reprogram cancer cells to undergo ferroptosis are considered effective drugs for cancer therapy. Here, we systematically summarize the molecular basis of ferroptosis, the suppressive effect of ferroptosis on tumors, the effect of ferroptosis on cellular metabolism and the tumor microenvironment (TME), and ferroptosis-inducing agents for tumor therapeutics. An understanding of the latest progress in ferroptosis could provide references for proposing new potential targets for the treatment of cancers.
Copyright © 2021. Published by Elsevier Inc.

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About The Expert

Haiyan Wang

Key Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078 China; NHC Key Laboratory of Carcinogenesis, Cancer Research Institute and School of Basic Medicine, Central South University, Changsha, Hunan, 410078 China.

Yan Cheng

Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, 410011 China.

Chao Mao

Key Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078 China; NHC Key Laboratory of Carcinogenesis, Cancer Research Institute and School of Basic Medicine, Central South University, Changsha, Hunan, 410078 China.

Shuang Liu

Department of Oncology, Institute of Medical Sciences, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, 410008 China. Electronic address: shuangliu2016@csu.edu.cn.

Desheng Xiao

Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008 China. Electronic address: xdsh96@csu.edu.cn.

Jun Huang

Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008 China. Electronic address: xyyyhj@csu.edu.cn.

Yongguang Tao

Key Laboratory of Carcinogenesis and Cancer Invasion (Central South University, Ministry of Education), Department of Pathology, Xiangya Hospital, Central South University, Hunan, 410078 China; NHC Key Laboratory of Carcinogenesis, Cancer Research Institute and School of Basic Medicine, Central South University, Changsha, Hunan, 410078 China; Hunan Key Laboratory of Early Diagnosis and Precision Therapy, Department of Thoracic Surgery, Second Xiangya Hospital, Central South University, Changsha 410011 China. Electronic address: taoyong@csu.edu.cn.

References

PubMed