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    A component of the mir-17-92 polycistronic oncomir promotes oncogene-dependent apoptosis

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    Author
    Olive, V; Sabio, E; Bennett, MJ; De Jong, CS; Biton, A; McGann, JC; Greaney, SK; Sodir, NM; Zhou, AY; Balakrishnan, A; ...
    Date
    2013-10-15
    Source Title
    eLife
    Publisher
    ELIFE SCIENCES PUBLICATIONS LTD
    University of Melbourne Author/s
    Speed, Terence
    Affiliation
    School of Mathematics and Statistics
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Olive, 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 Status
    Open Access
    URI
    http://hdl.handle.net/11343/259471
    DOI
    10.7554/eLife.00822
    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 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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