دورية أكاديمية
أعرض في EDS

FGF2-FGFR1 signaling regulates release of Leukemia-Protective exosomes from bone marrow stromal cells.

التفاصيل البيبلوغرافية
العنوان: FGF2-FGFR1 signaling regulates release of Leukemia-Protective exosomes from bone marrow stromal cells.
المؤلفون: Javidi-Sharifi N; Knight Cancer Institute, Oregon Health & Science University, Portland, United States., Martinez J; Knight Cancer Institute, Oregon Health & Science University, Portland, United States., English I; Knight Cancer Institute, Oregon Health & Science University, Portland, United States., Joshi SK; Knight Cancer Institute, Oregon Health & Science University, Portland, United States., Scopim-Ribeiro R; Knight Cancer Institute, Oregon Health & Science University, Portland, United States., Viola SK; Knight Cancer Institute, Oregon Health & Science University, Portland, United States., Edwards DK 5th; Knight Cancer Institute, Oregon Health & Science University, Portland, United States., Agarwal A; Knight Cancer Institute, Oregon Health & Science University, Portland, United States.; Division of Hematology and Medical Oncology, Oregon Health & Science University, Portland, United States., Lopez C; Knight Cancer Institute, Oregon Health & Science University, Portland, United States.; Center for Spatial Systems Biomedicine, Oregon Health & Science University, Portland, United States., Jorgens D; Knight Cancer Institute, Oregon Health & Science University, Portland, United States.; Center for Spatial Systems Biomedicine, Oregon Health & Science University, Portland, United States., Tyner JW; Knight Cancer Institute, Oregon Health & Science University, Portland, United States.; Department of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, United States., Druker BJ; Knight Cancer Institute, Oregon Health & Science University, Portland, United States.; Division of Hematology and Medical Oncology, Oregon Health & Science University, Portland, United States.; Howard Hughes Medical Institute, Chevy Chase, United States., Traer E; Knight Cancer Institute, Oregon Health & Science University, Portland, United States.; Division of Hematology and Medical Oncology, Oregon Health & Science University, Portland, United States.
المصدر: ELife [Elife] 2019 Feb 05; Vol. 8. Date of Electronic Publication: 2019 Feb 05.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: eLife Sciences Publications, Ltd Country of Publication: England NLM ID: 101579614 Publication Model: Electronic Cited Medium: Internet ISSN: 2050-084X (Electronic) Linking ISSN: 2050084X NLM ISO Abbreviation: Elife Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Cambridge, UK : eLife Sciences Publications, Ltd., 2012-
مواضيع طبية MeSH: Signal Transduction*, Exosomes/*metabolism , Fibroblast Growth Factor 2/*metabolism , Leukemia, Myeloid, Acute/*pathology , Mesenchymal Stem Cells/*metabolism , Receptor, Fibroblast Growth Factor, Type 1/*metabolism, Animals ; Cell Survival ; Cells, Cultured ; Disease Models, Animal ; Humans ; Mice ; Mice, Knockout
مستخلص: Protective signaling from the leukemia microenvironment leads to leukemia cell persistence, development of resistance, and disease relapse. Here, we demonstrate that fibroblast growth factor 2 (FGF2) from bone marrow stromal cells is secreted in exosomes, which are subsequently endocytosed by leukemia cells, and protect leukemia cells from tyrosine kinase inhibitors (TKIs). Expression of FGF2 and its receptor, FGFR1, are both increased in a subset of stromal cell lines and primary AML stroma; and increased FGF2/FGFR1 signaling is associated with increased exosome secretion. FGFR inhibition (or gene silencing) interrupts stromal autocrine growth and significantly decreases secretion of FGF2-containing exosomes, resulting in less stromal protection of leukemia cells. Likewise, Fgf2 -/- mice transplanted with retroviral BCR-ABL leukemia survive significantly longer than their +/+ counterparts when treated with TKI. Thus, inhibition of FGFR can modulate stromal function, reduce exosome secretion, and may be a therapeutic option to overcome resistance to TKIs.
Editorial Note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (see decision letter).
Competing Interests: NJ, JM, IE, SJ, RS, DE, AA, CL, DJ, JT, ET No competing interests declared, BD Is currently principal investigator or co-investigator on Novartis clinical trials. His institution, OHSU, has contracts with these companies to pay for patient costs, nurse and data manager salaries, and institutional overhead. He does not derive salary, nor does his lab receive funds from these contracts.
(© 2019, Javidi-Sharifi et al.)
التعليقات: Erratum in: Elife. 2019 Mar 29;8:. (PMID: 30924767)
References: J Biol Chem. 2015 Feb 6;290(6):3654-65. (PMID: 25533462)
Blood. 2017 Jul 6;130(1):48-58. (PMID: 28490572)
Br J Haematol. 2014 Jan;164(1):61-72. (PMID: 24116827)
Int J Mol Med. 2008 Jan;21(1):63-7. (PMID: 18097617)
Nature. 2012 Apr 15;485(7397):260-3. (PMID: 22504184)
Cancer Res. 2003 Nov 1;63(21):7241-6. (PMID: 14612519)
J Mol Biol. 2015 Mar 27;427(6 Pt A):1202-10. (PMID: 25051502)
J Control Release. 2016 Jan 28;222:107-15. (PMID: 26699421)
Drug Resist Updat. 2009 Jun;12(3):81-9. (PMID: 19467916)
Cancer. 2002 Nov 1;95(9):1923-30. (PMID: 12404286)
Blood. 2001 Feb 1;97(3):729-36. (PMID: 11157491)
Jpn J Cancer Res. 2002 Apr;93(4):459-66. (PMID: 11985797)
J Biol Chem. 2004 Feb 20;279(8):6244-51. (PMID: 14645213)
Blood Cancer J. 2015 Apr 10;5:e302. (PMID: 25860293)
Blood. 1994 Apr 15;83(8):2126-32. (PMID: 8161781)
Blood. 2012 Aug 30;120(9):1831-42. (PMID: 22802336)
Nat Rev Immunol. 2002 Aug;2(8):569-79. (PMID: 12154376)
Blood. 2011 Jun 23;117(25):6801-12. (PMID: 21527526)
Blood. 2016 Jul 14;128(2):253-64. (PMID: 27257182)
Oncogenesis. 2013 Mar 25;2:e39. (PMID: 23552882)
J Med Chem. 2011 Oct 27;54(20):7066-83. (PMID: 21936542)
Leukemia. 2008 Dec;22(12):2269-72. (PMID: 18509354)
Cancer Res. 2016 Nov 15;76(22):6471-6482. (PMID: 27671675)
Leukemia. 2009 Dec;23(12):2233-41. (PMID: 19727127)
J Cell Biochem. 2008 Apr 15;103(6):1783-97. (PMID: 17910038)
Nat Methods. 2012 Jun 28;9(7):676-82. (PMID: 22743772)
Blood. 1995 Feb 15;85(4):997-1005. (PMID: 7849321)
Hematol Oncol Clin North Am. 2017 Aug;31(4):681-692. (PMID: 28673395)
Blood. 1995 Sep 15;86(6):2123-9. (PMID: 7662960)
Exp Cell Res. 2008 Oct 1;314(16):2907-18. (PMID: 18687326)
Blood. 2014 Mar 6;123(10):1516-24. (PMID: 24408322)
Blood. 2009 Oct 1;114(14):2984-92. (PMID: 19654408)
Science. 2008 Dec 19;322(5909):1861-5. (PMID: 19095944)
Blood. 2017 Oct 5;130(14):1649-1660. (PMID: 28733324)
Nat Methods. 2014 Aug;11(8):783-784. (PMID: 25075903)
Cancer Res. 2011 Jun 1;71(11):3831-40. (PMID: 21512135)
Leukemia. 2015 Dec;29(12):2285-95. (PMID: 26108689)
Br J Haematol. 2016 Mar;172(6):983-6. (PMID: 26095727)
Nat Med. 1998 Feb;4(2):201-7. (PMID: 9461194)
Blood. 2015 Aug 27;126(9):1106-17. (PMID: 26100252)
EMBO J. 1998 Oct 15;17(20):5896-904. (PMID: 9774334)
Nat Rev Cancer. 2009 Sep;9(9):665-74. (PMID: 19693095)
Nat Med. 2012 Jun;18(6):883-91. (PMID: 22635005)
Nature. 2012 Jul 26;487(7408):505-9. (PMID: 22763448)
Proteomics. 2014 Jun;14(12):1472-9. (PMID: 24733759)
Cancer Res. 2011 Jul 1;71(13):4696-706. (PMID: 21546568)
Leukemia. 2012 May;26(5):1140-3. (PMID: 22094585)
Mol Cancer Ther. 2008 May;7(5):1121-9. (PMID: 18445657)
Semin Cancer Biol. 2012 Aug;22(4):342-9. (PMID: 22369922)
Cancer Res. 2015 Mar 1;75(5):880-91. (PMID: 25432174)
Blood. 2000 Sep 15;96(6):2240-5. (PMID: 10979972)
Blood. 2012 Aug 30;120(9):1843-55. (PMID: 22645180)
Blood. 2004 May 1;103(9):3521-8. (PMID: 14715624)
Exp Cell Res. 2003 Jul 1;287(1):98-105. (PMID: 12799186)
معلومات مُعتمدة: 5F30CA186477-03 United States NH NIH HHS; U54 CA224019 United States CA NCI NIH HHS; F30 CA186477 United States CA NCI NIH HHS; U01 CA217862 United States CA NCI NIH HHS; R01 CA229875 United States CA NCI NIH HHS; F30 CA239335 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: FGF2; FGFR1; bone marrow stroma; cancer biology; drug resistance; exosomes; human; human biology; medicine; microenvironment; mouse
المشرفين على المادة: 103107-01-3 (Fibroblast Growth Factor 2)
EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1)
تواريخ الأحداث: Date Created: 20190206 Date Completed: 20200326 Latest Revision: 20240411
رمز التحديث: 20240411
مُعرف محوري في PubMed: PMC6363389
DOI: 10.7554/eLife.40033
PMID: 30720426
قاعدة البيانات: MEDLINE
الوصف
تدمد:2050-084X
DOI:10.7554/eLife.40033