Journal article
A component of the mir-17-92 polycistronic oncomir promotes oncogene-dependent apoptosis
V Olive, E Sabio, MJ Bennett, CS De Jong, A Biton, JC McGann, SK Greaney, NM Sodir, AY Zhou, A Balakrishnan, M Foth, MA Luftig, A Goga, TP Speed, Z Xuan, GI Evan, Y Wan, AC Minella, L He
Elife | ELIFE SCIENCES PUBLICATIONS LTD | Published : 2013
Abstract
mir-17-92, a potent polycistronic oncomir, encodes six mature miRNAs with complex modes of interactions. In the Eμ-myc Burkitt's lymphoma model, mir-17-92 exhibits potent oncogenic activity by repressing c-Myc-induced apoptosis, primarily through its miR-19 components. Surprisingly, mir-17-92 also encodes the miR-92 component that negatively regulates its oncogenic cooperation with c-Myc. This miR-92 effect is, at least in part, mediated by its direct repression of Fbw7, which promotes the proteosomal degradation of c-Myc. Thus, overexpressing miR-92 leads to aberrant c-Myc increase, imposing a strong coupling between excessive proliferation and p53-dependent apoptosis. Interestingly, miR-92..
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Funding Acknowledgements
American Cancer Society 123339-RSG-12-265-01-RMC Lin He National Cancer Institute R00 CA126186 Lin He The Leukemia and Lymphoma Society LLS, 3423-13 Virginie Olive National Instititute of Health F31 CA165825-02 Erich Sabio National Cancer Institute R01 CA139067 Lin He National Cancer Institute 1R21CA175560-01 Lin He National Institute of Health R01HL098608 Alex C Minella National Heart, Lung and Blood Institute R01HL098608 Alex C Minella US Department of Defense W81XWH-12-1-0272 Andrei Goga National Institutes of Health 5R01CA170447 Andrei Goga The Leukemia and Lymphoma Society LLS, 1531 Andrei Goga