标题:Regulation of the C/EBP alpha signaling pathway in acute myeloid leukemia (Review)
作者:Song, Guanhua;Wang, Lin;Bi, Kehong;Jiang, Guosheng
作者机构:[Song, G] Department of Hemato-Oncology, Institute of Basic Medicine, Shandong Academy of Medical Sciences, 18877 Jingshi Road, Jinan, Shandong, 25006 更多
通讯作者:Bi, K
通讯作者地址:[Bi, K]Shandong Univ, Qianfoshan Mt Hosp, Dept Hematol, Jingshi Rd, Jinan 250014, Shandong, Peoples R China.
来源:Oncology reports
出版年:2015
卷:33
期:5
页码:2099-2106
DOI:10.3892/or.2015.3848
关键词:C/EBP alpha;leukemia;differentiation;granulocyte;monocyte
摘要:The transcription factor CCAAT/enhancer binding protein a (C/EBP alpha), as a critical regulator of myeloid development, directs granulocyte and monocyte differentiation. Various mechanisms have been identified to explain how C/EBP alpha functions in patients with acute myeloid leukemia (AML). C/EBP alpha expression is suppressed as a result of common leukemia-associated genetic and epigenetic alterations such as AML1-ETO, RAR alpha-PLZF or gene promoter methylation. Recent data have shown that ubiquitination modification also contributes to its downregulation. In addition, 10-15% of patients with AML in an intermediate cytogenetic risk subgroup were characterized by mutations of the C/EBP alpha gene. As a transcription factor, C/EBP alpha can translocate into the nucleus and further regulate a variety of genes directly or indirectly, which are all key factors for cell differentiation. This review summarizes recent reports concerning the dysregulation of C/EBP alpha expression at various levels in human AML. The currently available data are persuasive evidence suggesting that impaired abnormal C/EBP alpha expression contributes to the development of AML, and restoration of C/EBP alpha expression as well as its function represents a promising target for novel therapeutic strategies in AML.
收录类别:SCOPUS;SCIE
WOS核心被引频次:2
Scopus被引频次:3
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84927130599&doi=10.3892%2for.2015.3848&partnerID=40&md5=832970a6a307262046a8abc2d656c4ba
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