Abstract
Acute myeloid leukemia (AML) remains a biologically heterogeneous disease with high morbidity and mortality under the existing treatment strategies. Our previous study showed that E2A might be a potential therapeutic target for AML, but the underlying mechanism was unclear. Here, we found that SDCBP2 might be a target gene of E2A through RNA-seq combined ChIP-seq screening. This was also demonstrated by Co-IP experiment. Furthermore, the expression of E2A and SDCBP2 were increased in both AML cell lines and patient samples. Downregulation of SDCBP2 expression suppressed proliferation and induced differentiation of AML cells. In human xenograft mouse leukemia model, inhibiton of SDCBP2 expression delayed AML progression. Overall, the above results confirmed that SDCBP2 might be a target gene of E2A and a potential therapeutic target for AML.
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