Journal
CANCER RESEARCH
Volume 77, Issue 21, Pages 5808-5819Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-16-2524
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Funding
- NIH [5R01 CA115729-05]
- National Cancer Institute
- SPORE in Brain Cancer [1P50 CA127001-06]
- Broach Foundation for Brain Cancer Research
- Elias Family Fund
- NIH/NCI [1UH2TR00943-01, 1 R01 CA182905-01]
- UT MD Anderson Cancer Center Brain SPORE [2P50CA127001]
- Gene Pennebaker Brain Cancer Fund
- Ben and Catherine Ivy Foundation
- Anthony Bullock III Foundation
- Brian McCulloch Fund
- Uncle Kory Foundation
- Jason & Priscilla Hiley Fund
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Tumor-stromal communications impact tumorigenesis in ways that are incompletely understood. Here, we show that glioma-associated human mesenchymal stem cells (GA-hMSC), a newly identified stromal component of glioblastoma, release exosomes that increase the proliferation and clonogenicity of tumor-initiating glioma stem-like cells (GSC). This event leads to a significantly greater tumor burden and decreased host survival compared with untreated GSCs in orthotopic xenografts. Analysis of the exosomal content identified miR-1587 as a mediator of the exosomal effects on GSCs, in part via downregulation of the tumor-suppressive nuclear receptor corepressor NCOR1. Our results illuminate the tumor-supporting role for GA-hMSCs by identifying GA-hMSC-derived exosomes in the intercellular transfer of specific miRNA that enhance the aggressiveness of glioblastoma. (C) 2017 AACR.
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