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SCFFBW7 regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction

Author

Listed:
  • Hiroyuki Inuzuka

    (Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA)

  • Shavali Shaik

    (Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA)

  • Ichiro Onoyama

    (Medical Institute of Bioregulation, Kyushu University, Fukuoka, Fukuoka 812-8582, Japan)

  • Daming Gao

    (Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA)

  • Alan Tseng

    (Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA)

  • Richard S. Maser

    (Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Harvard Medical School
    The Jackson Laboratory)

  • Bo Zhai

    (Harvard Medical School)

  • Lixin Wan

    (Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA)

  • Alejandro Gutierrez

    (Dana-Farber Cancer Institute, Harvard Medical School)

  • Alan W. Lau

    (Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA)

  • Yonghong Xiao

    (Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Harvard Medical School)

  • Amanda L. Christie

    (Dana-Farber Cancer Institute, Harvard Medical School
    Lurie Family Imaging Center, Dana-Farber Cancer Institute)

  • Jon Aster

    (Brigham and Women’s Hospital, Harvard Medical School)

  • Jeffrey Settleman

    (Massachusetts General Hospital Cancer Center, Harvard Medical School)

  • Steven P. Gygi

    (Harvard Medical School)

  • Andrew L. Kung

    (Dana-Farber Cancer Institute, Harvard Medical School
    Lurie Family Imaging Center, Dana-Farber Cancer Institute)

  • Thomas Look

    (Dana-Farber Cancer Institute, Harvard Medical School)

  • Keiichi I. Nakayama

    (Medical Institute of Bioregulation, Kyushu University, Fukuoka, Fukuoka 812-8582, Japan)

  • Ronald A. DePinho

    (Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Harvard Medical School)

  • Wenyi Wei

    (Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA)

Abstract

FBW7 acts by affecting apoptosis Loss of the tumour suppressor FBW7 is frequently observed in various types of human cancers, but its mechanism of action as a tumour suppressor remains unclear. Two groups demonstrate that in several cancer types, including ovarian cancer and T-cell leukaemias, the apoptosis regulator MCL1 is targeted for degradation by FBW7. Inuzuka et al. find that this mechanism can determine the response to drugs targeting BCL2 family apoptosis factors, and Wertz et al. show that it is activated during mitotic arrest and determines the response to anti-tubulin chemotherapeutics. Deletion or mutation of FBW7 in patients with cancer can therefore render tumours resistant to these therapies.

Suggested Citation

  • Hiroyuki Inuzuka & Shavali Shaik & Ichiro Onoyama & Daming Gao & Alan Tseng & Richard S. Maser & Bo Zhai & Lixin Wan & Alejandro Gutierrez & Alan W. Lau & Yonghong Xiao & Amanda L. Christie & Jon Aste, 2011. "SCFFBW7 regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction," Nature, Nature, vol. 471(7336), pages 104-109, March.
    • Handle: RePEc:nat:nature:v:471:y:2011:i:7336:d:10.1038_nature09732
    DOI: 10.1038/nature09732
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    Cited by:

    1. Jing Liu & Collin Tokheim & Jonathan D. Lee & Wenjian Gan & Brian J. North & X. Shirley Liu & Pier Paolo Pandolfi & Wenyi Wei, 2021. "Genetic fusions favor tumorigenesis through degron loss in oncogenes," Nature Communications, Nature, vol. 12(1), pages 1-15, December.

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