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Bc13-dependent stabilization of CtBP1 is crucial for the inhibition of apoptosis and tumor progression in breast cancer

Cited 26 time in Web of Science Cited 28 time in Scopus
Authors
Choi, Hee June; Lee, Ji Min; Kim, Hyunkyung; Nam, Hye Jin; Kim, Dongha; Noh, Dong-Young; Kim, Jung Hwa; Baek, Sung Hee; Kim, Keun Il; Ko, Enyoung; Shin, Hi-Jai R.
Issue Date
2010-09-24
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS; Vol.400(3); 396-402
Keywords
Bcl3CtBP1UbiquitinationCancerApoptosis
Abstract
B-cell lymphoma 3 (Bcl3) is a proto-oncogene upregulated in a wide range of cancers, including breast cancer Although Bcl3 is known to promote cell proliferation and inhibit apoptosis, the molecular mechanisms underlying the proto-oncogenic function of Bcl3 have not been completely elucidated To gain insight into the oncogenic role of Bcl3, we applied a proteomic approach, which led to the identification of C-terminal binding protein 1 (CtBP1) as a binding partner of Bcl3 A PXDLS/R motif embedded in Bcl3 was found to mediate the interaction between Bcl3 and CtBP1, which caused the stabilization of CtBP1 by blocking proteasome-dependent degradation. Apoptotic stimuli-induced degradation of CtBP1 was significantly abolished by the upregulation of Bcl3, leading to the sustained repression of pro-apoptotic gene expression and subsequent inhibition of apoptosis. Intriguingly, a strong positive correlation between the protein levels of Bcl3 and CtBP1 was detected in breast cancer patient samples Our study reveals a novel combinatorial role for Bcl3 and CtBP1, providing an explanation for the acquisition of resistance to apoptosis in cancer cells, which is a major requirement for cancer development.
ISSN
0006-291X
Language
English
URI
http://hdl.handle.net/10371/77957
DOI
https://doi.org/10.1016/j.bbrc.2010.08.084
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College of Medicine/School of Medicine (의과대학/대학원)Surgery (외과학전공)Journal Papers (저널논문_외과학전공)
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