SEARCH:   Advanced

Blood, 15 January 2007, Vol. 109, No. 2, pp. 769-777. Prepublished online as a Blood First Edition Paper on September 21, 2006; DOI 10.1182/blood-2006-02-003517. This Article Full Text (PDF) All Versions of this Article: blood-2006-02-003517v1 109/2/769    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Ma, L.-H. Articles by Chen, S.-J. Search for Related Content PubMed PubMed Citation Articles by Ma, L.-H. Articles by Chen, S.-J. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 13, 2006 Accepted August 18, 2006 Aberrant transcriptional regulation of the MLL fusion partner EEN gene by AML1-ETO and its implication in leukemogenesis Li-Heng Ma, Han Liu, Hui Xiong, Bing Chen, Xiao-Wei Zhang, Yue-Ying Wang, Huang-Ying Le, Qiu-Hua Huang, Qing-Hua Zhang, Bo-Liang Li, Zhu Chen*, and Sai-Juan Chen State Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Shanghai, China Shanghai Laboratory of Disease and Health Genomics, Chinese National Human Genome Center at Shanghai Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Shanghai * Corresponding author; email: zchen{at}stn.sh.cn. EEN (extra eleven nineteen) gene located on chromosome 19p13 was cloned as a fusion with MLL from an acute myeloid leukemia (AML) patient with translocation t(11;19)(q23;p13). In this study, we characterized the genomic structure of EEN gene including its 5' regulatory region and transcription start site (TSS). We found that Sp1 could bind to the GC-stretch of EEN promoter and was critical for the normal EEN expression, while the leukemia associated fusion protein AML1-ETO could aberrantly transactivate EEN gene through an AML1 binding site. Of note, overexpressed EEN showed oncogenic properties, such as transforming potential in NIH3T3 cells, stimulating cell proliferation and increasing the activity of transcriptional factor AP-1. Retroviral transduction of EEN increased self-renewal and proliferation of murine hematopoietic progenitor cells. Moreover, Kasumi-1 and HL60 cell growth was inhibited with down regulation of EEN by RNAi. These findings demonstrate that EEN might be a common target in two major types of AML associated with MLL or AML1 translocations, and over-expression of EEN may play an essential role in leukemogenesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H.-Y. Le, Y. Zhang, H. Liu, L.-H. Ma, Y. Jin, Q.-H. Huang, Y. Chen, M. Deng, Z. Chen, S.-J. Chen, et al. eena Promotes Myeloid Proliferation through Stimulating ERK1/2 Phosphorylation in Zebrafish J. Biol. Chem., June 20, 2008; 283(25): 17652 - 17661. [Abstract] [Full Text] [PDF]

	Copyright © 2006 by American Society of Hematology         Online ISSN: 1528-0020