Ferroptosis, a novel pharmacological mechanism of anti-cancer drugs

Ferroptosis, a form of regulated cell death, is initiated by oxidative perturbations of the intracellular microenvironment, which is under the constitutive control of glutathione peroxidase 4 (GPX4). Ferrous iron (Fe2+) accumulation and lipid peroxidation are critical events in the induction of ferr...

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Vydáno v:	Cancer letters Ročník 483; s. 127 - 136
Hlavní autoři:	Su, Yanwei, Zhao, Bin, Zhou, Liangfu, Zhang, Zheyuan, Shen, Ying, Lv, Huanhuan, AlQudsy, Luban Hamdy Hameed, Shang, Peng
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Ireland Elsevier B.V 28.07.2020 Elsevier Limited
Témata:	Acetaminophen Alcohol Amino acids Animals Antibiotics Antineoplastic Agents - therapeutic use Antioxidants Apoptosis Artesunate Autophagy Cancer Cancer therapies Cell death Cell proliferation Chelating agents Cisplatin Drug development Fatty acids Ferritinophagy Ferroptosis Ferroptosis - drug effects Fibroblasts Free radicals Glutathione Glutathione peroxidase Glutathione peroxidase 4 Humans Immunomodulators Inhibitor drugs Iron Lipid peroxidation Lipid Peroxidation - drug effects Lipids Lipophilic Metabolism Mitochondria Morphology Neoplasms - drug therapy Neoplasms - metabolism Neoplasms - pathology Oxidation Oxidative Stress - drug effects Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Roles Salinomycin Signal Transduction Sulfasalazine System xc Targeted cancer therapy Tumor Microenvironment Vitamin E System xc Ferritinophagy Reactive oxygen species Iron Glutathione peroxidase 4 System x(c)(-)
ISSN:	0304-3835, 1872-7980, 1872-7980
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Popis
Shrnutí:	Ferroptosis, a form of regulated cell death, is initiated by oxidative perturbations of the intracellular microenvironment, which is under the constitutive control of glutathione peroxidase 4 (GPX4). Ferrous iron (Fe2+) accumulation and lipid peroxidation are critical events in the induction of ferroptosis, which is inhibited by iron chelators and lipophilic antioxidants. Ferroptosis terminates in mitochondrial dysfunction and toxic lipid peroxidation. It plays a vital role in inhibiting cancer growth and proliferation. It can be induced in cancer cells, and certain normal cells, by experimental compounds (e.g., erastin, Ras-selective lethal small molecule 3) or clinical drugs. The purpose of this review is to summarize the various drugs (e.g., sulfasalazine, lanperisone, sorafenib, fenugreek (trigonelline), acetaminophen, cisplatin, artesunate, combination of siramesine and lapatinib, ferumoxytol, and salinomycin (ironomycin)) that could induce ferroptosis in cancer cells and provide an overview of current knowledge regarding the mechanisms underlying ferroptosis. In future, we anticipate the development of more ferroptosis-inducing drugs, and the availability of such drugs for the clinical treatment of cancer. •We listed ten anticancer drugs related to ferroptosis.•We focused on the novel mechanisms of pharmacology of ten drugs.•We summarized all the current mechanisms related to ferroptosis.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23
ISSN:	0304-3835 1872-7980 1872-7980
DOI:	10.1016/j.canlet.2020.02.015