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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 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 Citation Map 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. Related Collections Neoplasia Oncogenes and Tumor Suppressors Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Aberrant transcriptional regulation of the MLL fusion partner EEN by AML1-ETO and its implication in leukemogenesis Li-Heng Ma1,2, Han Liu1, Hui Xiong3, Bing Chen1, Xiao-Wei Zhang1, Yue-Ying Wang1, Huang-Ying Le1, Qiu-Hua Huang1, Qing-Hua Zhang1, Bo-Liang Li4, Zhu Chen1,2, and Sai-Juan Chen1,2, 1 State Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital affiliated to School of Medicine, Shanghai Jiao Tong University (SJTU), Shanghai, China; 2 Shanghai Center for Systems Biomedicine, SJTU, Shanghai, China; 3 Shanghai Laboratory of Disease and Health Genomics, Chinese National Human Genome Center at Shanghai; 4 Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China The EEN (extra eleven nineteen) gene, located on chromosome 19p13, was cloned as a fusion with MLL from a patient with acute myeloid leukemia (AML) with translocation t(11;19)(q23;p13). In this study, we characterized the genomic structure of the EEN gene, including its 5' regulatory region and transcription start site (TSS). We found that Sp1 could bind to the guanine-cytosine (GC)–stretch of the EEN promoter and was critical for the normal EEN expression, whereas the leukemia-associated fusion protein AML1-ETO could aberrantly transactivate the 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 2 major types of AML associated with MLL or AML1 translocations, and overexpression 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]

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