Document Detail

BM mesenchymal stromal cell-derived exosomes facilitate multiple myeloma progression.
MedLine Citation:
PMID:  23454749     Owner:  NLM     Status:  MEDLINE    
BM mesenchymal stromal cells (BM-MSCs) support multiple myeloma (MM) cell growth, but little is known about the putative mechanisms by which the BM microenvironment plays an oncogenic role in this disease. Cell-cell communication is mediated by exosomes. In this study, we showed that MM BM-MSCs release exosomes that are transferred to MM cells, thereby resulting in modulation of tumor growth in vivo. Exosomal microRNA (miR) content differed between MM and normal BM-MSCs, with a lower content of the tumor suppressor miR-15a. In addition, MM BM-MSC-derived exosomes had higher levels of oncogenic proteins, cytokines, and adhesion molecules compared with exosomes from the cells of origin. Importantly, whereas MM BM-MSC-derived exosomes promoted MM tumor growth, normal BM-MSC exosomes inhibited the growth of MM cells. In summary, these in vitro and in vivo studies demonstrated that exosome transfer from BM-MSCs to clonal plasma cells represents a previously undescribed and unique mechanism that highlights the contribution of BM-MSCs to MM disease progression.
Aldo M Roccaro; Antonio Sacco; Patricia Maiso; Abdel Kareem Azab; Yu-Tzu Tai; Michaela Reagan; Feda Azab; Ludmila M Flores; Federico Campigotto; Edie Weller; Kenneth C Anderson; David T Scadden; Irene M Ghobrial
Related Documents :
23543769 - Il-4rα on cd4+ t cells plays a pathogenic role in respiratory syncytial virus reinfect...
24817389 - Current status of cell-mediated regenerative therapies for human spinal cord injury.
15215169 - Adult-derived liver stem cells acquire a cardiomyocyte structural and functional phenot...
22959759 - Follicular t-cell lymphoma: a member of an emerging family of follicular helper t-cell ...
23638139 - An efficient weighted graph strategy to identify differentiation associated genes in em...
23968979 - Expansion of the nkg2c+ natural killer-cell subset is associated with high-risk carotid...
11934729 - Expression of st2 in helper t lymphocytes of malignant pleural effusions.
21314739 - Myeloid-derived suppressor cells: a double-edged sword?
18442329 - Have we reached the point for in vivo rejuvenation?
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  123     ISSN:  1558-8238     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-05-09     Completed Date:  2013-05-20     Revised Date:  2013-09-24    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1542-55     Citation Subset:  AIM; IM    
Dana-Farber Cancer Institute, Department of Medical Oncology, Harvard Medical School, Boston, Massachusetts 02215, USA.
Data Bank Information
Bank Name/Acc. No.:
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Bone Marrow Neoplasms / metabolism,  secondary*
Cell Movement
Cell Proliferation
Culture Media, Conditioned
Disease Progression
Exosomes / metabolism,  physiology*
Femur / pathology
Mesenchymal Stem Cell Transplantation
Mesenchymal Stromal Cells / metabolism*,  physiology
Mice, Inbred C57BL
Mice, SCID
MicroRNAs / genetics,  metabolism
Middle Aged
Multiple Myeloma / metabolism,  pathology*
Neoplasm Transplantation
Tissue Scaffolds
Tumor Burden
Tumor Cells, Cultured
Grant Support
P01 CA078378/CA/NCI NIH HHS; P01 CA155258/CA/NCI NIH HHS; P50 CA100707/CA/NCI NIH HHS; R01 CA050947/CA/NCI NIH HHS; R01 CA154648/CA/NCI NIH HHS; R01CA125690/CA/NCI NIH HHS; R01CA133799/CA/NCI NIH HHS; R01CA154648/CA/NCI NIH HHS; U01 HL100402/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Culture Media, Conditioned; 0/MIRN15 microRNA, human; 0/MicroRNAs
Erratum In:
J Clin Invest. 2013 Aug 1;123(8):3635

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth.
Next Document:  Blockade of individual Notch ligands and receptors controls graft-versus-host disease.