Journal
BLOOD ADVANCES
Volume 3, Issue 21, Pages 3228-3240Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/bloodadvances.2019000403
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Funding
- Ministry of Education, Culture, Sports, Science, and Technology [S1511011, 16K07183, 18K07244]
- Takeda Science Foundation [S1511011, 16K07183, 18K07244]
- Grants-in-Aid for Scientific Research [18K07244, 16K07183] Funding Source: KAKEN
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Bone marrow stromal cells (BMSCs) interact with multiple myeloma (MM) cells in the bone marrow and create a permissive microenvironment for MM cell proliferation and survival. In this study, we investigated the role of extracellular vesicles (EVs) from BMSCs derived from patients with MM (MM-BMSCs). EV-encapsulated miR-10a expression was high while intracellular miR-10a was low in MM-BMSCs. We therefore hypothesized that miR-10a was packaged into EVs that were actively released into the extracellular space. Inhibition of EV release resulted in accumulation of intracellular miR-10a, inhibition of cell proliferation, and induction of apoptosis in MM-BMSCs. In contrast, proliferation and apoptosis of BMSCs derived from healthy individuals were unaffected by inhibition of EV release. Furthermore, miR-10a derived from MM-BMSCs was transferred into MM cells via EVs and enhanced their proliferation. These results suggest that inhibition of EV release induced apoptosis in MM-BMSCs and inhibited MM cell proliferation, indicating a possible role for MM-BMSC-targeted therapy.
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