4.7 Article

A Numb-Mdm2 fuzzy complex reveals an isoform-specific involvement of Numb in breast cancer

期刊

JOURNAL OF CELL BIOLOGY
卷 217, 期 2, 页码 745-762

出版社

ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201709092

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资金

  1. Ministero della Salute [GR-2010-2308100]
  2. Associazione Italiana per la Ricerca sul Cancro [[IG] 11904, IG 18629, IG 14404, 18988, MCO 10.000]
  3. Italian Ministry of University and Scientific Research
  4. Italian Ministry of Health
  5. Monzino Foundation
  6. Deutsche Forschungsgemeinschaft [DFG SFB1035, GRK1721]
  7. Japanese Ministry of Education, Culture, Sports, Science and Technology [26119005]
  8. Japan Agency for Medical Research and Development
  9. Platform Project for Supporting Drug Discovery and Life Science Research of Nagoya University
  10. European Commission [FP7-PEOPLE-20112011-IIF 301193, Hsp90NMR]
  11. European Molecular Biology Organization [EMBO ALTF 1255-2011]
  12. Grants-in-Aid for Scientific Research [26119005] Funding Source: KAKEN

向作者/读者索取更多资源

Numb functions as an oncosuppressor by inhibiting Notch signaling and stabilizing p53. This latter effect depends on the interaction of Numb with Mdm2, the E3 ligase that ubiquitinates p53 and commits it to degradation. In breast cancer (BC), loss of Numb results in a reduction of p53-mediated responses including sensitivity to genotoxic drugs and maintenance of homeostasis in the stem cell compartment. In this study, we show that the Numb-Mdm2 interaction represents a fuzzy complex mediated by a short Numb sequence encompassing its alternatively spliced exon 3 (Ex3), which is necessary and sufficient to inhibit Mdm2 and prevent p53 degradation. Alterations in the Numb splicing pattern are critical in BC as shown by increased chemoresistance of tumors displaying reduced levels of Ex3-containing isoforms, an effect that could be mechanistically linked to diminished p53 levels. A reduced level of Ex3-less Numb isoforms independently predicts poor outcome in BCs harboring wild-type p53. Thus, we have uncovered an important mechanism of chemoresistance and progression in p53-competent BCs.

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