Shi Ting, Ye Xiujin
Department of Hematology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2018 May 25;47(5):552-557. doi: 10.3785/j.issn.1008-9292.2018.10.16.
The CCAAT enhancer binding protein α (C/EBP α:p42 and p30),which encoded by CCAAT enhancer binding protein α () gene,plays a pretty crucial role in the regulation of myeloid hematopoiesis.The disorder of CEBPA gene expression is an pivotal mechanism of acute myeloid leukemia (AML). The result of uncontrolled expression of C/EBP α gene is the over-expression of p30 and the incomplete loss of p42, both of which contribute to the occurrence of AML. Restoring the expression ratio of C/EBP α such as over-expression of p42 or blocking the carcinogenic pathway of p30 seems to be important for the treatment of AML caused by such causes. In order to better guide medical decision-making, this article reviews research progress on C/EBPα in the pathogenesis of AML.
CCAAT增强子结合蛋白α(C/EBPα:p42和p30)由CCAAT增强子结合蛋白α(CEBPA)基因编码,在髓系造血调控中起相当关键的作用。CEBPA基因表达紊乱是急性髓系白血病(AML)的关键机制。C/EBPα基因失控表达的结果是p30过度表达和p42完全缺失,这两者都促成了AML的发生。恢复C/EBPα的表达比例,如p42的过表达或阻断p30的致癌途径,似乎对治疗由此类原因引起的AML很重要。为了更好地指导医疗决策,本文综述了C/EBPα在AML发病机制中的研究进展。