C/EBPβ 与 MYB 合作维持 AML 细胞的致癌程序。
C/EBPβ cooperates with MYB to maintain the oncogenic program of AML cells.
出版信息
Oncotarget. 2023 Mar 11;14:174-177. doi: 10.18632/oncotarget.28377.
Abstract
Studies on the role of transcription factor MYB in acute myeloid leukemia (AML) have identified MYB as a key regulator of a transcriptional program for self-renewal of AML cells. Recent work summarized here has now highlighted the CCAAT-box/enhancer binding protein beta (C/EBPβ) as an essential factor and potential therapeutic target that cooperates with MYB and coactivator p300 in the maintenance of the leukemic cells.
摘要
关于转录因子 MYB 在急性髓系白血病（AML）中作用的研究已经将 MYB 确定为 AML 细胞自我更新的转录程序的关键调节因子。这里总结的最新研究成果强调了 CCAAT 盒/增强子结合蛋白 β（C/EBPβ）作为一个重要因素和潜在的治疗靶点，它与 MYB 和共激活因子 p300 合作维持白血病细胞。
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