作者: Hyog Young Kwon , Jeevisha Bajaj , Takahiro Ito , Allen Blevins , Takaaki Konuma
DOI: 10.1016/J.STEM.2015.06.006
关键词:
摘要: SUMMARY Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children frequently resistant to therapy. Thus, identifying signals needed for AML propagation a critical step toward developing new approaches treating this disease. Here, we show Tetraspanin 3 target of the RNA binding protein Musashi 2, which plays key role in AML. We generated Tspan3 knockout mice were born without overt defects. However, deletion impaired leukemia stem cell self-renewal disease markedly improved survival mouse models Additionally, inhibition blocked growth patient samples, suggesting also important human As part mechanism, deficiency disabled responses CXCL12/SDF-1 led defects localization within niche. These identify as regulator leukemias highlight oncogenesis.