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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| Veröffentlicht in: | Cancer letters 2020-07, Vol.483, p.127-136 |
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| container_title | Cancer letters |
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| creator | Su, Yanwei Zhao, Bin Zhou, Liangfu Zhang, Zheyuan Shen, Ying Lv, Huanhuan AlQudsy, Luban Hamdy Hameed Shang, Peng |
| description | 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. |
| doi_str_mv | 10.1016/j.canlet.2020.02.015 |
| format | Article |
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•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.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2020.02.015</identifier><identifier>PMID: 32067993</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Acetaminophen ; Alcohol ; Amino acids ; Animals ; 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 peroxidase ; Glutathione peroxidase 4 ; Humans ; 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 ; Tumor Microenvironment ; Vitamin E</subject><ispartof>Cancer letters, 2020-07, Vol.483, p.127-136</ispartof><rights>2020 Elsevier B.V.</rights><rights>Copyright © 2020 Elsevier B.V. All rights reserved.</rights><rights>2020. Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-c11cd702e698c4910082632c90e5d7bd16baf75c41295b6c025bb5fc75f294f33</citedby><cites>FETCH-LOGICAL-c441t-c11cd702e698c4910082632c90e5d7bd16baf75c41295b6c025bb5fc75f294f33</cites><orcidid>0000-0001-5418-6240</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2020.02.015$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32067993$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Su, Yanwei</creatorcontrib><creatorcontrib>Zhao, Bin</creatorcontrib><creatorcontrib>Zhou, Liangfu</creatorcontrib><creatorcontrib>Zhang, Zheyuan</creatorcontrib><creatorcontrib>Shen, Ying</creatorcontrib><creatorcontrib>Lv, Huanhuan</creatorcontrib><creatorcontrib>AlQudsy, Luban Hamdy Hameed</creatorcontrib><creatorcontrib>Shang, Peng</creatorcontrib><title>Ferroptosis, a novel pharmacological mechanism of anti-cancer drugs</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>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.</description><subject>Acetaminophen</subject><subject>Alcohol</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Artesunate</subject><subject>Autophagy</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Cell death</subject><subject>Cell proliferation</subject><subject>Chelating agents</subject><subject>Cisplatin</subject><subject>Drug development</subject><subject>Fatty acids</subject><subject>Ferritinophagy</subject><subject>Ferroptosis</subject><subject>Ferroptosis - drug effects</subject><subject>Fibroblasts</subject><subject>Free radicals</subject><subject>Glutathione peroxidase</subject><subject>Glutathione peroxidase 4</subject><subject>Humans</subject><subject>Iron</subject><subject>Lipid peroxidation</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Lipids</subject><subject>Lipophilic</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Morphology</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Oxidation</subject><subject>Oxidative Stress - drug effects</subject><subject>Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Roles</subject><subject>Salinomycin</subject><subject>Signal Transduction</subject><subject>Sulfasalazine</subject><subject>System xc</subject><subject>Tumor Microenvironment</subject><subject>Vitamin E</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LxDAURYMozjj6D0QKbm19-WrajSCDo8KAG12HNE1nUtqmJq3gv7dDR5eu3ubce3kHoWsMCQac3teJVl1jhoQAgQRIApifoCXOBIlFnsEpWgIFFtOM8gW6CKEGAM4EP0cLSiAVeU6XaL0x3rt-cMGGu0hFnfsyTdTvlW-Vdo3bWa2aqDV6rzob2shVkeoGG0_b2vio9OMuXKKzSjXBXB3vCn1snt7XL_H27fl1_biNNWN4iDXGuhRATJpnmuUYICMpJToHw0tRlDgtVCW4ZpjkvEg1EF4UvNKCVyRnFaUrdDv39t59jiYMsnaj76ZJSRjhaUaFYBPFZkp7F4I3ley9bZX_lhjkwZys5WxOHsxJIHIyN8VujuVj0ZryL_SragIeZsBML35Z42XQ1kwWSuuNHmTp7P8LPzc2f-w</recordid><startdate>20200728</startdate><enddate>20200728</enddate><creator>Su, Yanwei</creator><creator>Zhao, Bin</creator><creator>Zhou, Liangfu</creator><creator>Zhang, Zheyuan</creator><creator>Shen, Ying</creator><creator>Lv, Huanhuan</creator><creator>AlQudsy, Luban Hamdy Hameed</creator><creator>Shang, Peng</creator><general>Elsevier B.V</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><orcidid>https://orcid.org/0000-0001-5418-6240</orcidid></search><sort><creationdate>20200728</creationdate><title>Ferroptosis, a novel pharmacological mechanism of anti-cancer drugs</title><author>Su, Yanwei ; Zhao, Bin ; Zhou, Liangfu ; Zhang, Zheyuan ; Shen, Ying ; Lv, Huanhuan ; AlQudsy, Luban Hamdy Hameed ; Shang, Peng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-c11cd702e698c4910082632c90e5d7bd16baf75c41295b6c025bb5fc75f294f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acetaminophen</topic><topic>Alcohol</topic><topic>Amino acids</topic><topic>Animals</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Artesunate</topic><topic>Autophagy</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Cell death</topic><topic>Cell proliferation</topic><topic>Chelating agents</topic><topic>Cisplatin</topic><topic>Drug development</topic><topic>Fatty acids</topic><topic>Ferritinophagy</topic><topic>Ferroptosis</topic><topic>Ferroptosis - drug effects</topic><topic>Fibroblasts</topic><topic>Free radicals</topic><topic>Glutathione peroxidase</topic><topic>Glutathione peroxidase 4</topic><topic>Humans</topic><topic>Iron</topic><topic>Lipid peroxidation</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Lipids</topic><topic>Lipophilic</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Morphology</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Oxidation</topic><topic>Oxidative Stress - drug effects</topic><topic>Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Roles</topic><topic>Salinomycin</topic><topic>Signal Transduction</topic><topic>Sulfasalazine</topic><topic>System xc</topic><topic>Tumor Microenvironment</topic><topic>Vitamin E</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Su, Yanwei</creatorcontrib><creatorcontrib>Zhao, Bin</creatorcontrib><creatorcontrib>Zhou, Liangfu</creatorcontrib><creatorcontrib>Zhang, Zheyuan</creatorcontrib><creatorcontrib>Shen, Ying</creatorcontrib><creatorcontrib>Lv, Huanhuan</creatorcontrib><creatorcontrib>AlQudsy, Luban Hamdy Hameed</creatorcontrib><creatorcontrib>Shang, Peng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Su, Yanwei</au><au>Zhao, Bin</au><au>Zhou, Liangfu</au><au>Zhang, Zheyuan</au><au>Shen, Ying</au><au>Lv, Huanhuan</au><au>AlQudsy, Luban Hamdy Hameed</au><au>Shang, Peng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ferroptosis, a novel pharmacological mechanism of anti-cancer drugs</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2020-07-28</date><risdate>2020</risdate><volume>483</volume><spage>127</spage><epage>136</epage><pages>127-136</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>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.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>32067993</pmid><doi>10.1016/j.canlet.2020.02.015</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-5418-6240</orcidid></addata></record> |
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| subjects | Acetaminophen Alcohol Amino acids Animals 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 peroxidase Glutathione peroxidase 4 Humans 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 Tumor Microenvironment Vitamin E |
| title | Ferroptosis, a novel pharmacological mechanism of anti-cancer drugs |
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