<i>miR-15</i> and <i>miR-16</i> induce apoptosis by targeting BCL2
Amelia Cimmino(University of Ferrara), George A. Calin(University of Ferrara), Muller Fabbri(University of Ferrara), Marilena V. Iorio(University of Ferrara), Manuela Ferracin(University of Ferrara), Masayoshi Shimizu(University of Ferrara), Sylwia E. Wojcik(University of Ferrara), Rami I. Aqeilan(University of Ferrara), Simona Zupo(University of Ferrara), Mariella Dono(University of Ferrara), Laura Z. Rassenti(University of Ferrara), Hansjüerg Alder(University of Ferrara), Stefano Volinia(University of Ferrara), Chang‐Gong Liu(University of Ferrara), Thomas J. Kipps(University of Ferrara), Massimo Negrini(University of Ferrara), Carlo M. Croce(University of Ferrara)
Cited by 3,517Open Access
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.
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