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Blood, 15 November 2008, Vol. 112, No. 10, pp. 4202-4212. Prepublished online as a Blood First Edition Paper on August 19, 2008; DOI 10.1182/blood-2008-03-147645. This Article Full Text Full Text (PDF) Supplemental Tables and Figures All Versions of this Article: blood-2008-03-147645v1 112/10/4202    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 Sander, S. Articles by Wirth, T. Search for Related Content PubMed PubMed Citation Articles by Sander, S. Articles by Wirth, T. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA MYC stimulates EZH2 expression by repression of its negative regulator miR-26a Sandrine Sander1, Lars Bullinger2, Kay Klapproth1, Katja Fiedler1, Hans A. Kestler3,4, Thomas F. E. Barth5, Peter Möller5, Stephan Stilgenbauer2, Jonathan R. Pollack6, and Thomas Wirth1 1 Institute of Physiological Chemistry, 2 Department of Internal Medicine III, 3 Department of Internal Medicine I, 4 Department of Neural Information Processing, and 5 Department of Pathology, University of Ulm, Ulm, Germany; and 6 Department of Pathology, Stanford University, CA The MYC oncogene, which is commonly mutated/amplified in tumors, represents an important regulator of cell growth because of its ability to induce both proliferation and apoptosis. Recent evidence links MYC to altered miRNA expression, thereby suggesting that MYC-regulated miRNAs might contribute to tumorigenesis. To further analyze the impact of MYC-regulated miRNAs, we investigated a murine lymphoma model harboring the MYC transgene in a Tet-off system to control its expression. Microarray-based miRNA expression profiling revealed both known and novel MYC targets. Among the miRNAs repressed by MYC, we identified the potential tumor suppressor miR-26a, which possessed the ability to attenuate proliferation in MYC-dependent cells. Interestingly, miR-26a was also found to be deregulated in primary human Burkitt lymphoma samples, thereby probably being of clinical relevance. Although today only few miRNA targets have been identified in human disease, we could show that ectopic expression of miR-26a influenced cell cycle progression by targeting the bona fide oncogene EZH2, a Polycomb protein and global regulator of gene expression yet unknown to be regulated by miRNAs. Thus, in addition to directly targeting protein-coding genes, MYC modulates genes important to oncogenesis via deregulation of miRNAs, thereby vitally contributing to MYC-induced lymphomagenesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E. M. C. Ohlsson Teague, C. G. Print, and M. L. Hull The role of microRNAs in endometriosis and associated reproductive conditions Hum. Reprod. Update, September 22, 2009; (2009) dmp034v1. [Abstract] [Full Text] [PDF] D. Sampath and W. Plunkett Response: Context-dependent actions of miR-106b in CLL Blood, June 18, 2009; 113(25): 6499 - 6500. [Full Text] [PDF] J. T. Huse, C. Brennan, D. Hambardzumyan, B. Wee, J. Pena, S. H. Rouhanifard, C. Sohn-Lee, C. le Sage, R. Agami, T. Tuschl, et al. The PTEN-regulating microRNA miR-26a is amplified in high-grade glioma and facilitates gliomagenesis in vivo Genes & Dev., June 1, 2009; 23(11): 1327 - 1337. [Abstract] [Full Text] [PDF]

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