دورية أكاديمية
أعرض في EDS

Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells.

التفاصيل البيبلوغرافية
العنوان: Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells.
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.
References: Cancer. 2011 Apr 15;117(8):1670-8. (PMID: 21472714)
Onco Targets Ther. 2018 Apr 13;11:2157-2167. (PMID: 29713184)
Nat Commun. 2015 Feb 05;6:6220. (PMID: 25653139)
Biochim Biophys Acta. 2011 Aug;1816(1):80-8. (PMID: 21586315)
Nature. 2015 Nov 12;527(7577):186-91. (PMID: 26466563)
PLoS One. 2014 May 23;9(5):e98479. (PMID: 24858344)
Nat Commun. 2018 Oct 26;9(1):4468. (PMID: 30367038)
PLoS One. 2012;7(12):e51703. (PMID: 23272146)
J Cell Sci. 2011 May 1;124(Pt 9):1396-402. (PMID: 21486948)
Neuroscience. 2015 Dec 17;311:398-414. (PMID: 26523980)
J Surg Oncol. 2009 Jun 1;99(7):424-7. (PMID: 19365809)
Cancer Res. 2018 May 15;78(10):2503-2512. (PMID: 29535219)
Anal Biochem. 1971 Nov;44(1):276-87. (PMID: 4943714)
Cell Rep. 2019 May 21;27(8):2292-2303.e6. (PMID: 31116976)
Oncogene. 2015 Jun;34(25):3315-24. (PMID: 25132267)
Lancet Oncol. 2006 Nov;7(11):925-34. (PMID: 17081918)
Int J Mol Sci. 2019 Jan 08;20(1):. (PMID: 30626133)
J Biol Chem. 2016 Feb 12;291(7):3268-79. (PMID: 26631723)
Nat Med. 2011 Oct 30;17(11):1498-503. (PMID: 22037646)
Oncogene. 2011 Jun 30;30(26):2986-96. (PMID: 21358671)
Biochem Biophys Res Commun. 2014 Jan 3;443(1):156-60. (PMID: 24287180)
CA Cancer J Clin. 2018 Jul;68(4):284-296. (PMID: 29809280)
Sci Transl Med. 2015 Oct 7;7(308):308re8. (PMID: 26446958)
Antioxidants (Basel). 2017 Nov 03;6(4):. (PMID: 29099803)
Cancer Res. 2015 Nov 15;75(22):4973-84. (PMID: 26359457)
Cancer Cell. 2010 Jan 19;17(1):41-52. (PMID: 20129246)
Cancer Cell. 2011 Mar 8;19(3):416-28. (PMID: 21397863)
Redox Biol. 2019 Jul;25:101051. (PMID: 30509602)
Cancer Cell. 2019 Jun 10;35(6):916-931.e9. (PMID: 31185214)
Cancer Res. 2013 Jun 15;73(12):3704-15. (PMID: 23771908)
Free Radic Biol Med. 2014 Nov;76:163-172. (PMID: 25152236)
Cell Metab. 2010 Dec 1;12(6):662-7. (PMID: 21109198)
Cancer Res. 2019 Apr 1;79(7):1369-1382. (PMID: 30683653)
Biochem Biophys Res Commun. 2016 Jul 1;475(3):245-50. (PMID: 27216459)
Diabetes. 2013 Oct;62(10):3404-17. (PMID: 23835326)
Cancer Res. 2017 Aug 1;77(15):3990-3999. (PMID: 28536275)
Nature. 2016 Apr 14;532(7598):255-8. (PMID: 27049945)
Oncogene. 2017 Aug;36(31):4393-4404. (PMID: 28368421)
Cancer. 2012 Dec 1;118(23):5800-10. (PMID: 22674009)
Carcinogenesis. 2012 Jan;33(1):49-58. (PMID: 22045027)
EMBO Rep. 2011 Jun;12(6):534-41. (PMID: 21566644)
PLoS One. 2015 Jun 29;10(6):e0131344. (PMID: 26121130)
Nature. 2009 Sep 3;461(7260):109-13. (PMID: 19693011)
Free Radic Biol Med. 2009 Jan 1;46(1):42-50. (PMID: 18930813)
Int J Oncol. 2016 Aug;49(2):773-84. (PMID: 27277143)
Cancer Res. 2007 Nov 1;67(21):10260-7. (PMID: 17974967)
Hum Pathol. 2014 May;45(5):1071-7. (PMID: 24746213)
Mol Cell. 2010 Dec 22;40(6):893-904. (PMID: 21172655)
Anticancer Agents Med Chem. 2011 Feb;11(2):191-201. (PMID: 21434856)
Nat Protoc. 2006;1(6):2643-9. (PMID: 17406520)
Clin Exp Metastasis. 2012 Apr;29(4):293-313. (PMID: 22249415)
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
الوصف
تدمد:1476-5594
DOI:10.1038/s41388-019-1097-7