PINK1 and PARK2 Suppress Pancreatic Tumorigenesis through Control of Mitochondrial Iron-Mediated Immunometabolism
Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic tumorigenesis through control of mitochondrial iron-dependent immunometabolism. Using mouse models of spontaneous pancreatic cancer, we show that...
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| Published in | Developmental cell Vol. 46; no. 4; pp. 441 - 455.e8 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
20.08.2018
Elsevier |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic tumorigenesis through control of mitochondrial iron-dependent immunometabolism. Using mouse models of spontaneous pancreatic cancer, we show that depletion of Pink1 and Park2 accelerates mutant Kras-driven pancreatic tumorigenesis. PINK1-PARK2 pathway-mediated degradation of SLC25A37 and SLC25A28 increases mitochondrial iron accumulation, which leads to the HIF1A-dependent Warburg effect and AIM2-dependent inflammasome activation in tumor cells. AIM2-mediated HMGB1 release further induces expression of CD274/PD-L1. Consequently, pharmacological administration of mitochondrial iron chelator, anti-HMGB1 antibody, or genetic depletion of Hif1a or Aim2 in pink1−/− and park2−/− mice confers protection against pancreatic tumorigenesis. Low PARK2 expression and high SLC25A37 and AIM2 expression are associated with poor prognosis in patients with pancreatic cancer. These findings suggest that disrupted mitochondrial iron homeostasis may contribute to cancer development and hence constitute a target for therapeutic intervention.
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•PINK1 and PARK2 suppress oncogenic Kras-driven pancreatic tumorigenesis•Mitochondrial iron accumulation contributes to pancreatic tumorigenesis•HIF1A is required for the Warburg effect in pancreatic tumorigenesis•AIM2-mediated HMGB1 release promotes pancreatic tumorigenesis
Li et al. demonstrate in mouse models that Pink1 and Park2 deficiency accelerates pancreatic tumorigenesis through mitochondrial iron-dependent immunometabolic dysfunction. These findings shed light on how the autophagy pathway controls iron homeostasis and could have implications for the development of strategies to target mitochondrial iron metabolism in pancreatic cancer. |
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| AbstractList | Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic tumorigenesis through control of mitochondrial iron-dependent immunometabolism. Using mouse models of spontaneous pancreatic cancer, we show that depletion of Pink1 and Park2 accelerates mutant Kras-driven pancreatic tumorigenesis. PINK1-PARK2 pathway-mediated degradation of SLC25A37 and SLC25A28 increases mitochondrial iron accumulation, which leads to the HIF1A-dependent Warburg effect and AIM2-dependent inflammasome activation in tumor cells. AIM2-mediated HMGB1 release further induces expression of CD274/PD-L1. Consequently, pharmacological administration of mitochondrial iron chelator, anti-HMGB1 antibody, or genetic depletion of Hif1a or Aim2 in pink1-/- and park2-/- mice confers protection against pancreatic tumorigenesis. Low PARK2 expression and high SLC25A37 and AIM2 expression are associated with poor prognosis in patients with pancreatic cancer. These findings suggest that disrupted mitochondrial iron homeostasis may contribute to cancer development and hence constitute a target for therapeutic intervention.Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic tumorigenesis through control of mitochondrial iron-dependent immunometabolism. Using mouse models of spontaneous pancreatic cancer, we show that depletion of Pink1 and Park2 accelerates mutant Kras-driven pancreatic tumorigenesis. PINK1-PARK2 pathway-mediated degradation of SLC25A37 and SLC25A28 increases mitochondrial iron accumulation, which leads to the HIF1A-dependent Warburg effect and AIM2-dependent inflammasome activation in tumor cells. AIM2-mediated HMGB1 release further induces expression of CD274/PD-L1. Consequently, pharmacological administration of mitochondrial iron chelator, anti-HMGB1 antibody, or genetic depletion of Hif1a or Aim2 in pink1-/- and park2-/- mice confers protection against pancreatic tumorigenesis. Low PARK2 expression and high SLC25A37 and AIM2 expression are associated with poor prognosis in patients with pancreatic cancer. These findings suggest that disrupted mitochondrial iron homeostasis may contribute to cancer development and hence constitute a target for therapeutic intervention. Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic tumorigenesis through control of mitochondrial iron-dependent immunometabolism. Using mouse models of spontaneous pancreatic cancer, we show that depletion of Pink1 and Park2 accelerates mutant Kras-driven pancreatic tumorigenesis. PINK1-PARK2 pathway-mediated degradation of SLC25A37 and SLC25A28 increases mitochondrial iron accumulation, which leads to the HIF1A-dependent Warburg effect and AIM2-dependent inflammasome activation in tumor cells. AIM2-mediated HMGB1 release further induces expression of CD274/PD-L1. Consequently, pharmacological administration of mitochondrial iron chelator, anti-HMGB1 antibody, or genetic depletion of Hif1a or Aim2 in pink1[-/-] and park2[-/-] mice confers protection against pancreatic tumorigenesis. Low PARK2 expression and high SLC25A37 and AIM2 expression are associated with poor prognosis in patients with pancreatic cancer. These findings suggest that disrupted mitochondrial iron homeostasis may contribute to cancer development and hence constitute a target for therapeutic intervention. Copyright © 2018 Elsevier Inc. All rights reserved. Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic tumorigenesis through control of mitochondrial iron-dependent immunometabolism. Using mouse models of spontaneous pancreatic cancer, we show that depletion of Pink1 and Park2 accelerates mutant Kras-driven pancreatic tumorigenesis. PINK1-PARK2 pathway-mediated degradation of SLC25A37 and SLC25A28 increases mitochondrial iron accumulation, which leads to the HIF1A-dependent Warburg effect and AIM2-dependent inflammasome activation in tumor cells. AIM2-mediated HMGB1 release further induces expression of CD274/PD-L1. Consequently, pharmacological administration of mitochondrial iron chelator, anti-HMGB1 antibody, or genetic depletion of Hif1a or Aim2 in pink1−/− and park2−/− mice confers protection against pancreatic tumorigenesis. Low PARK2 expression and high SLC25A37 and AIM2 expression are associated with poor prognosis in patients with pancreatic cancer. These findings suggest that disrupted mitochondrial iron homeostasis may contribute to cancer development and hence constitute a target for therapeutic intervention. [Display omitted] •PINK1 and PARK2 suppress oncogenic Kras-driven pancreatic tumorigenesis•Mitochondrial iron accumulation contributes to pancreatic tumorigenesis•HIF1A is required for the Warburg effect in pancreatic tumorigenesis•AIM2-mediated HMGB1 release promotes pancreatic tumorigenesis Li et al. demonstrate in mouse models that Pink1 and Park2 deficiency accelerates pancreatic tumorigenesis through mitochondrial iron-dependent immunometabolic dysfunction. These findings shed light on how the autophagy pathway controls iron homeostasis and could have implications for the development of strategies to target mitochondrial iron metabolism in pancreatic cancer. Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic tumorigenesis through control of mitochondrial iron-dependent immunometabolism. Using mouse models of spontaneous pancreatic cancer, we show that depletion of Pink1 and Park2 accelerates mutant Kras -driven pancreatic tumorigenesis. PINK1-PARK2 pathway-mediated degradation of SLC25A37 and SLC25A28 increases mitochondrial iron accumulation, which leads to the HIF1A-dependent Warburg effect and AIM2-dependent inflammasome activation in tumor cells. AIM2-mediated HMGB1 release further induces expression of CD274/PD-L1. Consequently, pharmacological administration of mitochondrial iron chelator, anti-HMGB1 antibody, or genetic depletion of Hif1a or Aim2 in pink1 −/− and park2 −/− mice confers protection against pancreatic tumorigenesis. Low PARK2 expression and high SLC25A37 and AIM2 expression are associated with poor prognosis in patients with pancreatic cancer. These findings suggest that disrupted mitochondrial iron homeostasis may contribute to cancer development and hence constitute a target for therapeutic intervention. Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic tumorigenesis through control of mitochondrial iron-dependent immunometabolism. Using mouse models of spontaneous pancreatic cancer, we show that depletion of Pink1 and Park2 accelerates mutant Kras-driven pancreatic tumorigenesis. PINK1-PARK2 pathway-mediated degradation of SLC25A37 and SLC25A28 increases mitochondrial iron accumulation, which leads to the HIF1A-dependent Warburg effect and AIM2-dependent inflammasome activation in tumor cells. AIM2-mediated HMGB1 release further induces expression of CD274/PD-L1. Consequently, pharmacological administration of mitochondrial iron chelator, anti-HMGB1 antibody, or genetic depletion of Hif1a or Aim2 in pink1 and park2 mice confers protection against pancreatic tumorigenesis. Low PARK2 expression and high SLC25A37 and AIM2 expression are associated with poor prognosis in patients with pancreatic cancer. These findings suggest that disrupted mitochondrial iron homeostasis may contribute to cancer development and hence constitute a target for therapeutic intervention. |
| Author | Tang, Daolin Cheng, Xing Xie, Yangchun Lotze, Michael T. Liu, Jinbao Wen, Qirong Kang, Rui Klionsky, Daniel J. Li, Changfeng Yuan, Hua Zhang, Ying Liu, Jiao Zeh, Herbert J. Zhu, Shan Kroemer, Guido |
| AuthorAffiliation | 6 Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers; 75006 Paris, France 11 Department of Women's and Children's Health, Karolinska University Hospital, 17176 Stockholm, Sweden 7 Institut National de la Santé et de la Recherche Médicale, U1138; Paris, France 8 Université Pierre et Marie Curie, 75006 Paris, France 13 Lead Contact 4 Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA 10 Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP; 75015 Paris, France 2 School of Nursing of Jilin University, Changchun, Jilin 130021, China 12 Life Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI USA 3 The Third Affiliated Hospital, Center for DAMP Biology, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Key Laboratory of Protein Modification and Degradation of Guangdong Higher Education Institutes, School of Basic Medical Sciences, Guangz |
| AuthorAffiliation_xml | – name: 6 Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers; 75006 Paris, France – name: 12 Life Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI USA – name: 3 The Third Affiliated Hospital, Center for DAMP Biology, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Key Laboratory of Protein Modification and Degradation of Guangdong Higher Education Institutes, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 510510, China – name: 13 Lead Contact – name: 11 Department of Women's and Children's Health, Karolinska University Hospital, 17176 Stockholm, Sweden – name: 8 Université Pierre et Marie Curie, 75006 Paris, France – name: 10 Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP; 75015 Paris, France – name: 7 Institut National de la Santé et de la Recherche Médicale, U1138; Paris, France – name: 1 Department of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, China – name: 9 Metabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus; 94800 Villejuif, France – name: 2 School of Nursing of Jilin University, Changchun, Jilin 130021, China – name: 4 Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA – name: 5 Université Paris Descartes, Sorbonne Paris Cité; 75006 Paris, France |
| Author_xml | – sequence: 1 givenname: Changfeng surname: Li fullname: Li, Changfeng email: changfengli1975@sina.com organization: Department of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, China – sequence: 2 givenname: Ying surname: Zhang fullname: Zhang, Ying organization: Department of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, China – sequence: 3 givenname: Xing surname: Cheng fullname: Cheng, Xing organization: Department of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, China – sequence: 4 givenname: Hua surname: Yuan fullname: Yuan, Hua organization: School of Nursing of Jilin University, Changchun, Jilin 130021, China – sequence: 5 givenname: Shan surname: Zhu fullname: Zhu, Shan organization: The Third Affiliated Hospital, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 510510, China – sequence: 6 givenname: Jiao surname: Liu fullname: Liu, Jiao organization: The Third Affiliated Hospital, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 510510, China – sequence: 7 givenname: Qirong surname: Wen fullname: Wen, Qirong organization: The Third Affiliated Hospital, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 510510, China – sequence: 8 givenname: Yangchun surname: Xie fullname: Xie, Yangchun organization: Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15213, USA – sequence: 9 givenname: Jinbao surname: Liu fullname: Liu, Jinbao organization: The Third Affiliated Hospital, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 510510, China – sequence: 10 givenname: Guido surname: Kroemer fullname: Kroemer, Guido organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 11 givenname: Daniel J. surname: Klionsky fullname: Klionsky, Daniel J. organization: Life Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, USA – sequence: 12 givenname: Michael T. surname: Lotze fullname: Lotze, Michael T. organization: Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15213, USA – sequence: 13 givenname: Herbert J. surname: Zeh fullname: Zeh, Herbert J. organization: Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15213, USA – sequence: 14 givenname: Rui surname: Kang fullname: Kang, Rui organization: Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15213, USA – sequence: 15 givenname: Daolin surname: Tang fullname: Tang, Daolin email: tangd2@upmc.edu organization: The Third Affiliated Hospital, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 510510, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30100261$$D View this record in MEDLINE/PubMed https://hal.science/hal-04702756$$DView record in HAL |
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| ContentType | Journal Article |
| Copyright | 2018 Elsevier Inc. Copyright © 2018 Elsevier Inc. All rights reserved. Distributed under a Creative Commons Attribution 4.0 International License |
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| Issue | 4 |
| Keywords | pink1 park2 aim2 mitochondrial quality control mitophagy inflammasomes pancreatic tumorigenesis iron immunosuppression hmgb1 |
| Language | English |
| License | This article is made available under the Elsevier license. Copyright © 2018 Elsevier Inc. All rights reserved. Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 D.T. and C.L. designed the experiments. C.L., Y.Z., X.C., H.Y., S.Z., J.L., Q.W., Y.X., J.L., R.K., and D.T conducted the experiments. D.T. and C.L. wrote the paper. M.T.L. and H.J.Z. provided the reagents. G.K. and D.J.K. edited and commented on the manuscript. Author Contributions |
| OpenAccessLink | https://www.sciencedirect.com/science/article/pii/S1534580718305975 |
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| PublicationDate | 2018-08-20 |
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| PublicationTitle | Developmental cell |
| PublicationTitleAlternate | Dev Cell |
| PublicationYear | 2018 |
| Publisher | Elsevier Inc Elsevier |
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| Snippet | Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic... Pancreatic cancer is an aggressive malignancy with changes in the tumor microenvironment. Here, we demonstrate that PINK1 and PARK2 suppressed pancreatic... |
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| SubjectTerms | aim2 Animals Autophagy - physiology Carcinogenesis - metabolism Cell Transformation, Neoplastic - pathology hmgb1 immunosuppression inflammasomes iron Iron - metabolism Life Sciences Mice, Transgenic Mitochondria - genetics Mitochondria - metabolism Mitochondrial Proteins - metabolism mitochondrial quality control mitophagy Mitophagy - genetics pancreatic tumorigenesis park2 pink1 Protein Kinases - genetics Protein Kinases - metabolism Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism |
| Title | PINK1 and PARK2 Suppress Pancreatic Tumorigenesis through Control of Mitochondrial Iron-Mediated Immunometabolism |
| URI | https://dx.doi.org/10.1016/j.devcel.2018.07.012 https://www.ncbi.nlm.nih.gov/pubmed/30100261 https://www.proquest.com/docview/2087994714 https://hal.science/hal-04702756 https://pubmed.ncbi.nlm.nih.gov/PMC7654182 |
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