Zinc transporter ZIP7 is a novel determinant of ferroptosis
Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and membrane damages. The name of ferroptosis indicates that the ferroptotic death process depends on iron, but not other metals, as one of its canonical fe...
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Published in | Cell death & disease Vol. 12; no. 2; p. 198 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Nature Publishing Group UK
19.02.2021
Springer Nature B.V Nature Publishing Group |
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Abstract | Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and membrane damages. The name of ferroptosis indicates that the ferroptotic death process depends on iron, but not other metals, as one of its canonical features. Here, we reported that zinc is also essential for ferroptosis in breast and renal cancer cells. Zinc chelator suppressed ferroptosis, and zinc addition promoted ferroptosis, even during iron chelation. By interrogating zinc-related genes in a genome-wide RNAi screen of ferroptosis, we identified
SLC39A7
, encoding ZIP7 that controls zinc transport from endoplasmic reticulum (ER) to cytosol, as a novel genetic determinant of ferroptosis. Genetic and chemical inhibition of the ZIP7 protected cells against ferroptosis, and the ferroptosis protection upon ZIP7 knockdown can be abolished by zinc supplementation. We found that the genetic and chemical inhibition of ZIP7 triggered ER stresses, including the induction of the expression of
HERPUD1
and
ATF3
. Importantly, the knockdown of
HERPUD1
abolished the ferroptosis protection phenotypes of ZIP7 inhibition. Together, we have uncovered an unexpected role of ZIP7 in ferroptosis by maintaining ER homeostasis. These findings may have therapeutic implications for human diseases involving ferroptosis and zinc dysregulations. |
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AbstractList | Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and membrane damages. The name of ferroptosis indicates that the ferroptotic death process depends on iron, but not other metals, as one of its canonical features. Here, we reported that zinc is also essential for ferroptosis in breast and renal cancer cells. Zinc chelator suppressed ferroptosis, and zinc addition promoted ferroptosis, even during iron chelation. By interrogating zinc-related genes in a genome-wide RNAi screen of ferroptosis, we identified SLC39A7, encoding ZIP7 that controls zinc transport from endoplasmic reticulum (ER) to cytosol, as a novel genetic determinant of ferroptosis. Genetic and chemical inhibition of the ZIP7 protected cells against ferroptosis, and the ferroptosis protection upon ZIP7 knockdown can be abolished by zinc supplementation. We found that the genetic and chemical inhibition of ZIP7 triggered ER stresses, including the induction of the expression of HERPUD1 and ATF3. Importantly, the knockdown of HERPUD1 abolished the ferroptosis protection phenotypes of ZIP7 inhibition. Together, we have uncovered an unexpected role of ZIP7 in ferroptosis by maintaining ER homeostasis. These findings may have therapeutic implications for human diseases involving ferroptosis and zinc dysregulations. Abstract Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and membrane damages. The name of ferroptosis indicates that the ferroptotic death process depends on iron, but not other metals, as one of its canonical features. Here, we reported that zinc is also essential for ferroptosis in breast and renal cancer cells. Zinc chelator suppressed ferroptosis, and zinc addition promoted ferroptosis, even during iron chelation. By interrogating zinc-related genes in a genome-wide RNAi screen of ferroptosis, we identified SLC39A7, encoding ZIP7 that controls zinc transport from endoplasmic reticulum (ER) to cytosol, as a novel genetic determinant of ferroptosis. Genetic and chemical inhibition of the ZIP7 protected cells against ferroptosis, and the ferroptosis protection upon ZIP7 knockdown can be abolished by zinc supplementation. We found that the genetic and chemical inhibition of ZIP7 triggered ER stresses, including the induction of the expression of HERPUD1 and ATF3. Importantly, the knockdown of HERPUD1 abolished the ferroptosis protection phenotypes of ZIP7 inhibition. Together, we have uncovered an unexpected role of ZIP7 in ferroptosis by maintaining ER homeostasis. These findings may have therapeutic implications for human diseases involving ferroptosis and zinc dysregulations. Abstract Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and membrane damages. The name of ferroptosis indicates that the ferroptotic death process depends on iron, but not other metals, as one of its canonical features. Here, we reported that zinc is also essential for ferroptosis in breast and renal cancer cells. Zinc chelator suppressed ferroptosis, and zinc addition promoted ferroptosis, even during iron chelation. By interrogating zinc-related genes in a genome-wide RNAi screen of ferroptosis, we identified SLC39A7 , encoding ZIP7 that controls zinc transport from endoplasmic reticulum (ER) to cytosol, as a novel genetic determinant of ferroptosis. Genetic and chemical inhibition of the ZIP7 protected cells against ferroptosis, and the ferroptosis protection upon ZIP7 knockdown can be abolished by zinc supplementation. We found that the genetic and chemical inhibition of ZIP7 triggered ER stresses, including the induction of the expression of HERPUD1 and ATF3 . Importantly, the knockdown of HERPUD1 abolished the ferroptosis protection phenotypes of ZIP7 inhibition. Together, we have uncovered an unexpected role of ZIP7 in ferroptosis by maintaining ER homeostasis. These findings may have therapeutic implications for human diseases involving ferroptosis and zinc dysregulations. Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and membrane damages. The name of ferroptosis indicates that the ferroptotic death process depends on iron, but not other metals, as one of its canonical features. Here, we reported that zinc is also essential for ferroptosis in breast and renal cancer cells. Zinc chelator suppressed ferroptosis, and zinc addition promoted ferroptosis, even during iron chelation. By interrogating zinc-related genes in a genome-wide RNAi screen of ferroptosis, we identified SLC39A7 , encoding ZIP7 that controls zinc transport from endoplasmic reticulum (ER) to cytosol, as a novel genetic determinant of ferroptosis. Genetic and chemical inhibition of the ZIP7 protected cells against ferroptosis, and the ferroptosis protection upon ZIP7 knockdown can be abolished by zinc supplementation. We found that the genetic and chemical inhibition of ZIP7 triggered ER stresses, including the induction of the expression of HERPUD1 and ATF3 . Importantly, the knockdown of HERPUD1 abolished the ferroptosis protection phenotypes of ZIP7 inhibition. Together, we have uncovered an unexpected role of ZIP7 in ferroptosis by maintaining ER homeostasis. These findings may have therapeutic implications for human diseases involving ferroptosis and zinc dysregulations. |
ArticleNumber | 198 |
Author | Chen, Po-Han Yang, Wen-Hsuan Wu, Jianli Xu, Yitong Ding, Chien-Kuang Cornelia Chi, Jen-Tsan Mestre, Alexander A. Lin, Chao-Chieh |
Author_xml | – sequence: 1 givenname: Po-Han orcidid: 0000-0002-9471-4471 surname: Chen fullname: Chen, Po-Han organization: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Duke Center for Genomic and Computational Biology, Duke University – sequence: 2 givenname: Jianli surname: Wu fullname: Wu, Jianli organization: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Duke Center for Genomic and Computational Biology, Duke University – sequence: 3 givenname: Yitong surname: Xu fullname: Xu, Yitong organization: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Duke Center for Genomic and Computational Biology, Duke University – sequence: 4 givenname: Chien-Kuang Cornelia surname: Ding fullname: Ding, Chien-Kuang Cornelia organization: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Duke Center for Genomic and Computational Biology, Duke University – sequence: 5 givenname: Alexander A. surname: Mestre fullname: Mestre, Alexander A. organization: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Duke Center for Genomic and Computational Biology, Duke University, Department of Biochemistry, Duke University Medical Center – sequence: 6 givenname: Chao-Chieh orcidid: 0000-0001-5890-9004 surname: Lin fullname: Lin, Chao-Chieh organization: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Duke Center for Genomic and Computational Biology, Duke University – sequence: 7 givenname: Wen-Hsuan orcidid: 0000-0001-5780-6839 surname: Yang fullname: Yang, Wen-Hsuan organization: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Duke Center for Genomic and Computational Biology, Duke University, Department of Biochemistry, Duke University Medical Center – sequence: 8 givenname: Jen-Tsan orcidid: 0000-0003-3433-903X surname: Chi fullname: Chi, Jen-Tsan email: jentsan.chi@duke.edu organization: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Duke Center for Genomic and Computational Biology, Duke University |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33608508$$D View this record in MEDLINE/PubMed |
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Snippet | Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and membrane... Abstract Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and... Abstract Ferroptosis is a newly described form of regulated cell death triggered by oxidative stresses and characterized by extensive lipid peroxidation and... |
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SubjectTerms | 13 38 38/89 38/91 631/337/2019 631/80/82/23 631/80/82/2344 Activating transcription factor 3 Antibodies Biochemistry Biomedical and Life Sciences Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - metabolism Carcinoma, Renal Cell - pathology Cation Transport Proteins - antagonists & inhibitors Cation Transport Proteins - genetics Cation Transport Proteins - metabolism Cell Biology Cell Culture Cell death Cell Line, Tumor Chelating Agents - pharmacology Chelation Cytosol Endoplasmic reticulum Endoplasmic Reticulum - genetics Endoplasmic Reticulum - metabolism Endoplasmic Reticulum - pathology Female Ferroptosis Ferroptosis - drug effects Gene Expression Regulation, Neoplastic Genomes Heavy metals Homeostasis Humans Immunology Iron Kidney cancer Kidney Neoplasms - genetics Kidney Neoplasms - metabolism Kidney Neoplasms - pathology Life Sciences Lipid peroxidation Membrane Proteins - genetics Membrane Proteins - metabolism Oxidative stress Phenotypes RNA-mediated interference Supplements Zinc Zinc - metabolism Zinc transporter |
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Title | Zinc transporter ZIP7 is a novel determinant of ferroptosis |
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