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<i>miR-15</i> and <i>miR-16</i> induce apoptosis by targeting BCL2

Proceedings of the National Academy of SciencesPublished 15 September 2005Open access
Amelia Cimmino, George A. Calin, Muller Fabbri, Marilena V. Iorio, Manuela Ferracin, Masayoshi Shimizu
Citations3,521
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TL;DR

It is demonstrated thatmiR-15a and miR-16-1 expression is inversely correlated to Bcl2 expression in CLL and that both microRNAs negatively regulate BCL2 at a posttranscriptional level and are natural antisense B cl2 interactors that could be used for therapy of Bcl1-overexpressing tumors.

Abstract

Chronic lymphocytic leukemia (CLL) is the most common human leukemia and is characterized by predominantly nondividing malignant B cells overexpressing the antiapoptotic B cell lymphoma 2 (Bcl2) protein. miR-15a and miR-16-1 are deleted or down-regulated in the majority of CLLs. Here, we demonstrate that miR-15a and miR-16-1 expression is inversely correlated to Bcl2 expression in CLL and that both microRNAs negatively regulate Bcl2 at a posttranscriptional level. BCL2 repression by these microRNAs induces apoptopsis in a leukemic cell line model. Therefore, miR-15 and miR-16 are natural antisense Bcl2 interactors that could be used for therapy of Bcl2-overexpressing tumors.

Keywords

Biochemistry, Genetics and Molecular Biology