SCFFBW7 regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction

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 Aster, Jeffrey Settleman, Steven P. Gygi, Andrew L. Kung, Thomas Look, Keiichi I. Nakayama, Ronald A. DePinho and Wenyi Wei ()
Additional contact information
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
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
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
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

Nature, 2011, vol. 471, issue 7336, 104-109

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.

Date: 2011
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DOI: 10.1038/nature09732

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