دورية أكاديمية
Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells.
العنوان: | Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells. |
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المؤلفون: | Kim YS; Department of Pharmacology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Gupta Vallur P; Department of Pharmacology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Jones VM; Department of Pharmacology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Worley BL; Department of Pharmacology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Shimko S; Department of Pharmacology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Shin DH; Department of Pharmacology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Crawford LC; Department of Pharmacology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Chen CW; Department of Cellular and Molecular Physiology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Aird KM; Department of Cellular and Molecular Physiology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Abraham T; Department of Neural and Behavioral Sciences, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Shepherd TG; The Mary & John Knight Translational Ovarian Cancer Research Unit, Departments of Obstetrics & Gynecology Oncology and Anatomy & Cell Biology, Western University, London, ON, Canada., Warrick JI; Department of Pathology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Lee NY; Department of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ, USA., Phaeton R; Department of Obstetrics and Gynecology, and Microbiology and Immunology, College of Medicine, Pennsylvania State University, Hershey, PA, USA., Mythreye K; Department of Chemistry and Biochemistry, University of South Carolina, Columbia, SC, USA. mythreye@uab.edu.; Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA. mythreye@uab.edu., Hempel N; Department of Pharmacology, College of Medicine, Pennsylvania State University, Hershey, PA, USA. nhempel@psu.edu. |
المصدر: | Oncogene [Oncogene] 2020 Feb; Vol. 39 (8), pp. 1619-1633. Date of Electronic Publication: 2019 Nov 13. |
نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. |
اللغة: | English |
بيانات الدورية: | Publisher: Nature Publishing Group Country of Publication: England NLM ID: 8711562 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5594 (Electronic) Linking ISSN: 09509232 NLM ISO Abbreviation: Oncogene Subsets: MEDLINE |
أسماء مطبوعة: | Publication: <2002->: Basingstoke : Nature Publishing Group Original Publication: Basingstoke, Hampshire, UK : Scientific & Medical Division, MacMillan Press, c1987- |
مواضيع طبية MeSH: | Ovarian Neoplasms/*pathology , Sirtuin 3/*metabolism, Cell Survival ; Enzyme Activation ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Glycolysis ; Humans ; Mitochondria/metabolism ; Neoplasm Metastasis ; Reactive Oxygen Species/metabolism ; Sirtuin 3/deficiency ; Sirtuin 3/genetics ; Superoxide Dismutase/metabolism |
مستخلص: | Tumor cells must alter their antioxidant capacity for maximal metastatic potential. Yet the antioxidant adaptations required for ovarian cancer transcoelomic metastasis, which is the passive dissemination of cells in the peritoneal cavity, remain largely unexplored. Somewhat contradicting the need for oxidant scavenging are previous observations that expression of SIRT3, a nutrient stress sensor and regulator of mitochondrial antioxidant defenses, is often suppressed in many primary tumors. We have discovered that this mitochondrial deacetylase is specifically upregulated in a context-dependent manner in cancer cells. SIRT3 activity and expression transiently increased following ovarian cancer cell detachment and in tumor cells derived from malignant ascites of high-grade serous adenocarcinoma patients. Mechanistically, SIRT3 prevents mitochondrial superoxide surges in detached cells by regulating the manganese superoxide dismutase (SOD2). This mitochondrial stress response is under dual regulation by SIRT3. SIRT3 rapidly increases SOD2 activity as an early adaptation to cellular detachment, which is followed by SIRT3-dependent increases in SOD2 mRNA during sustained anchorage-independence. In addition, SIRT3 inhibits glycolytic capacity in anchorage-independent cells thereby contributing to metabolic changes in response to detachment. While manipulation of SIRT3 expression has few deleterious effects on cancer cells in attached conditions, SIRT3 upregulation and SIRT3-mediated oxidant scavenging are required for anoikis resistance in vitro following matrix detachment, and both SIRT3 and SOD2 are necessary for colonization of the peritoneal cavity in vivo. Our results highlight the novel context-specific, pro-metastatic role of SIRT3 in ovarian cancer. |
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معلومات مُعتمدة: | S10 OD018124 United States OD NIH HHS; R01 CA230628 United States CA NCI NIH HHS; TL1 TR002016 United States TR NCATS NIH HHS; UL1 TR002014 United States TR NCATS NIH HHS; R00 CA143229 United States CA NCI NIH HHS; R01 GM128055 United States GM NIGMS NIH HHS |
المشرفين على المادة: | 0 (Reactive Oxygen Species) EC 1.15.1.1 (Superoxide Dismutase) EC 1.15.1.1 (superoxide dismutase 2) EC 3.5.1.- (Sirtuin 3) |
تواريخ الأحداث: | Date Created: 20191115 Date Completed: 20201124 Latest Revision: 20231113 |
رمز التحديث: | 20231113 |
مُعرف محوري في PubMed: | PMC7036012 |
DOI: | 10.1038/s41388-019-1097-7 |
PMID: | 31723239 |
قاعدة البيانات: | MEDLINE |
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