دورية أكاديمية
أعرض في EDS

Circulating IGF-1 promotes prostate adenocarcinoma via FOXO3A/BIM signaling in a double-transgenic mouse model.

التفاصيل البيبلوغرافية
العنوان: Circulating IGF-1 promotes prostate adenocarcinoma via FOXO3A/BIM signaling in a double-transgenic mouse model.
المؤلفون: Wang S; Institute of Genome Engineered Animal Models for Human Diseases, Dalian Medical University, Dalian, Liaoning, 116044, China.; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian, Liaoning, 116044, China.; College of Integrative Medicine, Dalian Medical University, Dalian, Liaoning, 116044, China., Wang N; Institute of Genome Engineered Animal Models for Human Diseases, Dalian Medical University, Dalian, Liaoning, 116044, China.; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian, Liaoning, 116044, China.; College of Integrative Medicine, Dalian Medical University, Dalian, Liaoning, 116044, China., Yu B; Institute of Genome Engineered Animal Models for Human Diseases, Dalian Medical University, Dalian, Liaoning, 116044, China.; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian, Liaoning, 116044, China., Cao M; Institute of Genome Engineered Animal Models for Human Diseases, Dalian Medical University, Dalian, Liaoning, 116044, China.; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian, Liaoning, 116044, China.; College of Life Science and Technology, Mudanjiang Normal University, Mudanjiang, Heilongjiang, 157011, China., Wang Y; Department of Urology Surgery, Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian, Liaoning, 116033, China., Guo Y; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY, 10010, USA., Zhang Y; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY, 10010, USA., Zhang P; Department of Endocrinology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, 116027, China., Yu X; Department of Pathology, Dalian Medical University, Dalian, Liaoning, 116044, China., Wang S; Department of Biochemistry and Molecular Biology, Dalian Medical University, Dalian, Liaoning, 116044, China., Zeng L; Institute of Genome Engineered Animal Models for Human Diseases, Dalian Medical University, Dalian, Liaoning, 116044, China.; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian, Liaoning, 116044, China., Liang B; Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, CAS Center for Excellence in Animal Evolution and Genetics, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China. liangb@mail.kiz.ac.cn., Li X; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY, 10010, USA. xl15@nyu.edu.; Department of Urology, New York University Langone Medical Center, New York, NY, 10016, USA. xl15@nyu.edu.; Perlmutter Cancer Institute, New York University Langone Medical Center, New York, NY, 10016, USA. xl15@nyu.edu., Wu Y; Institute of Genome Engineered Animal Models for Human Diseases, Dalian Medical University, Dalian, Liaoning, 116044, China. yingjiewu@dmu.edu.cn.; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian, Liaoning, 116044, China. yingjiewu@dmu.edu.cn.; College of Integrative Medicine, Dalian Medical University, Dalian, Liaoning, 116044, China. yingjiewu@dmu.edu.cn.; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY, 10010, USA. yingjiewu@dmu.edu.cn.; Division of Endocrinology, Diabetes and Bone Disease, Department of Medicine, Icahn Mount Sinai School of Medicine, New York, NY, 10029, USA. yingjiewu@dmu.edu.cn.
المصدر: Oncogene [Oncogene] 2019 Sep; Vol. 38 (36), pp. 6338-6353. Date of Electronic Publication: 2019 Jul 16.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
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: Adenocarcinoma*/blood , Adenocarcinoma*/genetics , Adenocarcinoma*/pathology , Prostatic Neoplasms*/blood , Prostatic Neoplasms*/genetics , Prostatic Neoplasms*/pathology, Bcl-2-Like Protein 11/*physiology , Forkhead Box Protein O3/*physiology , Insulin-Like Growth Factor I/*physiology, Animals ; Bcl-2-Like Protein 11/genetics ; Cell Line, Tumor ; Cohort Studies ; Disease Models, Animal ; Disease Progression ; Forkhead Box Protein O3/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Insulin-Like Growth Factor I/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mice, Transgenic ; PC-3 Cells ; Signal Transduction/genetics
مستخلص: High circulating insulin-like growth factor-1 (IGF-1) levels increase the risk of prostate cancer. However, whether circulating IGF-1 levels directly aggravate prostate cancer remains elusive. In this study, we crossed a transgenic prostate adenocarcinoma mouse model, Hi-Myc mice, with a liver-specific IGF-1 transgenic mouse model (HIT) to increase their circulating IGF-1 levels to investigate the impact of the elevated circulating IGF-1 on prostate cancer development in vivo. The Hi-Myc/HIT mice had increased incidence and invasiveness of prostate cancer. IGF-1 elevation led to the accumulation of FOXO3A in the cytosol of prostate tumor cells and downregulation of its target gene Bim, which resulted in the apoptosis inhibition and prostate cancer overgrowth. The differential expressions of IGF-1R, FOXO3A, and BIM in the benign versus malignant prostate tissues supported a negative association between the FOXO3A/BIM axis and IGF-1R expression in human prostate adenocarcinoma. Our findings suggest that targeting the IGF-1/FOXO3A/BIM signaling axis could be an attractive strategy for prostate cancer prevention or treatment.
References: EMBO J. 1999 Nov 1;18(21):6027-36. (PMID: 10545114)
Curr Drug Targets. 2003 Apr;4(3):263-79. (PMID: 12643476)
Cancer Res. 2004 Mar 15;64(6):2270-305. (PMID: 15026373)
Biochim Biophys Acta Mol Basis Dis. 2018 May;1864(5 Pt A):1873-1882. (PMID: 29518496)
Endocrinology. 2009 Sep;150(9):4395-403. (PMID: 19497975)
Mol Cancer Res. 2005 Mar;3(3):163-9. (PMID: 15798096)
N Engl J Med. 2003 Jul 24;349(4):366-81. (PMID: 12878745)
Cancer Res. 2008 May 1;68(9):3495-504. (PMID: 18451178)
Cancer Cell. 2003 Sep;4(3):223-38. (PMID: 14522256)
Science. 1998 Aug 28;281(5381):1309-12. (PMID: 9721092)
Am J Surg Pathol. 2008 Dec;32(12):1890-5. (PMID: 18813120)
Prostate. 2017 Feb;77(2):145-153. (PMID: 27699813)
Cell Death Dis. 2016 Feb 25;7:e2111. (PMID: 26913603)
Cancer Metastasis Rev. 2014 Sep;33(2-3):377-97. (PMID: 24452759)
Br J Cancer. 1992 Mar;65(3):311-20. (PMID: 1313689)
Exp Diabesity Res. 2003 Oct-Dec;4(4):205-12. (PMID: 14668044)
Cancer Res. 2002 Feb 15;62(4):1030-5. (PMID: 11861378)
Cancer Res. 2014 May 15;74(10):2763-72. (PMID: 24686169)
Int J Cancer. 2015 May 15;136(10):2418-26. (PMID: 25348852)
Nature. 2009 Sep 24;461(7263):495-500. (PMID: 19741607)
Cancer Res. 2016 Apr 15;76(8):2288-2300. (PMID: 26921328)
Endocr Rev. 2007 Feb;28(1):20-47. (PMID: 16931767)
Endocrinology. 2010 Dec;151(12):5751-61. (PMID: 20926579)
Curr Diab Rep. 2009 Jun;9(3):208-14. (PMID: 19490822)
Oncogene. 2014 Aug 14;33(33):4213-25. (PMID: 24077289)
Stem Cells. 2013 Apr;31(4):627-40. (PMID: 23335250)
Curr Biol. 2000 Oct 5;10(19):1201-4. (PMID: 11050388)
CA Cancer J Clin. 2018 Jan;68(1):7-30. (PMID: 29313949)
Oncogene. 2008 May 1;27(20):2868-76. (PMID: 18026134)
Prostate. 2010 May 1;70(6):591-600. (PMID: 19938013)
Cancer Res. 1998 Jul 15;58(14):3021-7. (PMID: 9679966)
J Biol Chem. 2003 Dec 12;278(50):49795-805. (PMID: 14527951)
Int J Cancer. 2016 Oct 1;139(7):1520-33. (PMID: 27225428)
Prostate Cancer. 2017;2017:5687212. (PMID: 28168057)
J Biol Chem. 2005 Sep 30;280(39):33558-65. (PMID: 16061480)
Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3455-60. (PMID: 10737798)
Novartis Found Symp. 2004;262:3-9; discussion 9-18, 265-8. (PMID: 15562820)
Trends Cell Biol. 2008 Sep;18(9):421-9. (PMID: 18715783)
Urology. 2000 Sep 1;56(3):423-9. (PMID: 10962307)
Oncogene. 2005 Mar 31;24(14):2317-29. (PMID: 15688014)
Int J Cancer. 2007 Nov 15;121(10):2267-73. (PMID: 17597108)
Cancer Res. 2008 Sep 15;68(18):7661-9. (PMID: 18794155)
Nat Biotechnol. 2007 Mar;25(3):345-52. (PMID: 17322870)
المشرفين على المادة: 0 (Bcl-2-Like Protein 11)
0 (FOXO3 protein, human)
0 (Forkhead Box Protein O3)
0 (FoxO3 protein, mouse)
0 (IGF1 protein, human)
0 (insulin-like growth factor-1, mouse)
67763-96-6 (Insulin-Like Growth Factor I)
تواريخ الأحداث: Date Created: 20190718 Date Completed: 20200128 Latest Revision: 20210110
رمز التحديث: 20231215
DOI: 10.1038/s41388-019-0880-9
PMID: 31312023
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-5594
DOI:10.1038/s41388-019-0880-9