A component of the mir-17-92 polycistronic oncomir promotes oncogene-dependent apoptosis
Web of Science
AuthorOlive, V; Sabio, E; Bennett, MJ; De Jong, CS; Biton, A; McGann, JC; Greaney, SK; Sodir, NM; Zhou, AY; Balakrishnan, A; ...
PublisherELIFE SCIENCES PUBLICATIONS LTD
University of Melbourne Author/sSpeed, Terence
AffiliationSchool of Mathematics and Statistics
Document TypeJournal Article
CitationsOlive, V., Sabio, E., Bennett, M. J., De Jong, C. S., Biton, A., McGann, J. C., Greaney, S. K., Sodir, N. M., Zhou, A. Y., Balakrishnan, A., Foth, M., Luftig, M. A., Goga, A., Speed, T. P., Xuan, Z., Evan, G. I., Wan, Y., Minella, A. C. & He, L. (2013). A component of the mir-17-92 polycistronic oncomir promotes oncogene-dependent apoptosis. ELIFE, 2 (2), https://doi.org/10.7554/eLife.00822.
Access StatusOpen Access
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 antagonizes the oncogenic miR-19 miRNAs; and such functional interaction coordinates proliferation and apoptosis during c-Myc-induced oncogenesis. This miR-19:miR-92 antagonism is disrupted in B-lymphoma cells that favor a greater increase of miR-19 over miR-92. Altogether, we suggest a new paradigm whereby the unique gene structure of a polycistronic oncomir confers an intricate balance between oncogene and tumor suppressor crosstalk. DOI:http://dx.doi.org/10.7554/eLife.00822.001.
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