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Blood, 15 May 2007, Vol. 109, No. 10, pp. 4399-4405. Prepublished online as a Blood First Edition Paper on February 6, 2007; DOI 10.1182/blood-2006-09-045104. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-09-045104v1 109/10/4399    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 Venturini, L. Articles by Scherr, M. Search for Related Content PubMed PubMed Citation Articles by Venturini, L. Articles by Scherr, M. Related Collections Neoplasia Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Expression of the miR-17-92 polycistron in chronic myeloid leukemia (CML) CD34+ cells Letizia Venturini1, Karin Battmer1, Mirco Castoldi2, Beate Schultheis3, Andreas Hochhaus3, Martina U. Muckenthaler2, Arnold Ganser1, Matthias Eder1, and Michaela Scherr1 1 Department of Hematology, Hemostasis, and Oncology, Hannover Medical School, Germany; 2 Department of Pediatric Oncology, Hematology, and Immunology, University of Heidelberg, Germany; 3 III Medical Clinic, University Hospital of Mannheim, University of Heidelberg, Mannheim, Germany Aberrant micro RNA (miRNA) expression has been described in human malignancies including B-cell lymphomas. We here report BCR-ABL– and c-MYC–dependent regulation of miRNA expression in chronic myeloid leukemia (CML) using microarray analysis (miCHIP) and miRNA-specific quantitative real-time reverse transcriptase–polymerase chain reaction (miR-qRT-PCR). In 3 bcr-abl–positive cell lines, expression of miRNAs encoded within the polycistronic miR-17-92 cluster is specifically down-regulated (2- to 5-fold) by both imatinib treatment and anti–BCR-ABL RNA interference (RNAi). In addition, anti–c-MYC RNAi reduces miR-17-92 expression in K562 cells in which miRNAs can specifically repress reporter gene expression, as demonstrated by specific miRNA inhibition with antagomirs. Furthermore, lentivirus-mediated overexpression of polycistronic miRNAs in K562 cells confers increased proliferation, partial resistance against anti–c-MYC RNAi, and enhanced sensitivity to imatinib-induced cell death. Finally, we determined miR-17-92 expression in purified normal (n = 4), early chronic-phase (CP) (n = 24), and blast-crisis (BC) (n = 7) CML CD34+ cells and found up-regulation of polycistronic pri-miRNA transcripts in CML and mature miRNAs in CP but not in BC CML. These data are in accordance with a BCR-ABL–c-MYC–miR-17-92 pathway that mediates enhanced miRNA expression in CP but not BC CML CD34+ cells. Altered miRNA expression may contribute to the pathophysiology of the disease and may provide potential targets for therapeutic intervention. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: I. Manni, S. Artuso, S. Careccia, M. G. Rizzo, R. Baserga, G. Piaggio, and A. Sacchi The microRNA miR-92 increases proliferation of myeloid cells and by targeting p63 modulates the abundance of its isoforms FASEB J, November 1, 2009; 23(11): 3957 - 3966. [Abstract] [Full Text] [PDF] M. Raponi, L. Dossey, T. Jatkoe, X. Wu, G. Chen, H. Fan, and D. G. Beer MicroRNA Classifiers for Predicting Prognosis of Squamous Cell Lung Cancer Cancer Res., July 15, 2009; 69(14): 5776 - 5783. [Abstract] [Full Text] [PDF] A. Bonauer, G. Carmona, M. Iwasaki, M. Mione, M. Koyanagi, A. Fischer, J. Burchfield, H. Fox, C. Doebele, K. Ohtani, et al. MicroRNA-92a Controls Angiogenesis and Functional Recovery of Ischemic Tissues in Mice Science, June 26, 2009; 324(5935): 1710 - 1713. [Abstract] [Full Text] [PDF] X. Agirre, A. Jimenez-Velasco, E. San Jose-Eneriz, L. Garate, E. Bandres, L. Cordeu, O. Aparicio, B. Saez, G. Navarro, A. Vilas-Zornoza, et al. Down-Regulation of hsa-miR-10a in Chronic Myeloid Leukemia CD34+ Cells Increases USF2-Mediated Cell Growth Mol. Cancer Res., December 1, 2008; 6(12): 1830 - 1840. [Abstract] [Full Text] [PDF] C. Urbich, A. Kuehbacher, and S. Dimmeler Role of microRNAs in vascular diseases, inflammation, and angiogenesis Cardiovasc Res, September 1, 2008; 79(4): 581 - 588. [Abstract] [Full Text] [PDF] T. Schepeler, J. T. Reinert, M. S. Ostenfeld, L. L. Christensen, A. N. Silahtaroglu, L. Dyrskjot, C. Wiuf, F. J. Sorensen, M. Kruhoffer, S. Laurberg, et al. Diagnostic and Prognostic MicroRNAs in Stage II Colon Cancer Cancer Res., August 1, 2008; 68(15): 6416 - 6424. [Abstract] [Full Text] [PDF] H. Bruchova, M. Merkerova, and J. T. Prchal Aberrant expression of microRNA in polycythemia vera Haematologica, July 1, 2008; 93(7): 1009 - 1016. [Abstract] [Full Text] [PDF] M. Scherr, L. Venturini, K. Battmer, M. Schaller-Schoenitz, D. Schaefer, I. Dallmann, A. Ganser, and M. Eder Lentivirus-mediated antagomir expression for specific inhibition of miRNA function Nucleic Acids Res., December 3, 2007; 35(22): e149 - e149. [Abstract] [Full Text] [PDF]

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