Journal
CELL STEM CELL
Volume 17, Issue 2, Pages 152-164Publisher
CELL PRESS
DOI: 10.1016/j.stem.2015.06.006
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Funding
- National Cancer Center
- California Institute for Regenerative Medicine interdisciplinary stem cell training program fellowship
- Japanese Society for the Promotion of Science
- NIH Pharmacological Sciences Training Program [T32 GM007752]
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [2014R1A1A2A16052133]
- Lymphoma and Leukemia Society Scholar Award
- University of California San Diego Moores Cancer Center NCI Core Grant [P30CA23100]
- NIH [HL097767, DP1 CA174422, DK099335, CA186043]
- National Research Foundation of Korea [2014R1A1A2A16052133] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children and is frequently resistant to therapy. Thus, identifying signals needed for AML propagation is a critical step toward developing new approaches for treating this disease. Here, we show that Tetraspanin 3 is a target of the RNA binding protein Musashi 2, which plays a key role in AML. We generated Tspan3 knockout mice that were born without overt defects. However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML. Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease. As part of the mechanism, we show that Tspan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the niche. These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis.
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