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Long non-coding RNAs in leukemia: biology and clinical impact.白血病中的长链非编码RNA：生物学特性与临床影响
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CCAAT增强子结合蛋白α在急性髓细胞白血病中的作用

[Roles of CCAAT enhancer binding protein α in acute myeloblastic leukemia].

作者信息

Shi Ting, Ye Xiujin

机构信息

Department of Hematology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.

出版信息

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.

DOI:10.3785/j.issn.1008-9292.2018.10.16
PMID:30693699
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10393672/
Abstract

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.

摘要

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。