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Tcl1 Expression in Chronic Lymphocytic Leukemia Is Regulated by miR-29 and miR-181

¹ Comprehensive Cancer Center, Human Cancer Genetics Program and Department of Molecular Virology, Immunology, and Medical Genetics, OSU School of Medicine, Ohio State University, Columbus, Ohio; and ² Department of Medicine, University of California at San Diego, La Jolla, California

Requests for reprints: Yuri Pekarsky, Comprehensive Cancer Center, Ohio State University, 410 West 12th Avenue, 435 Wiseman Hall, Columbus, OH 43210. Phone: 614-292-3120; Fax: 614-292-3312; E-mail: Pekarsky.Yuri{at}osumc.edu.

B-cell chronic lymphocytic leukemia (B-CLL) is the most common human leukemia in the world. Deregulation of the TCL1 oncogene is a causal event in the pathogenesis of the aggressive form of this disease as was verified by using animal models. To study the mechanism of Tcl1 regulation in CLL, we carried out microRNA expression profiling of three types of CLL: indolent CLL, aggressive CLL, and aggressive CLL showing 11q deletion. We identified distinct microRNA signatures corresponding to each group of CLL. We further determined that Tcl1 expression is regulated by miR-29 and miR-181, two microRNAs differentially expressed in CLL. Expression levels of miR-29 and miR-181 generally inversely correlated with Tcl1 expression in the CLL samples we examined. Our results suggest that Tcl1 expression in CLL is, at least in part, regulated by miR-29 and miR-181 and that these microRNAs may be candidates for therapeutic agents in CLLs overexpressing Tcl1. (Cancer Res 2006; 66(24): 11590-3)

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