Bc13-dependent stabilization of CtBP1 is crucial for the inhibition of apoptosis and tumor progression in breast cancer
- Authors
- Choi, Hee June; Lee, Ji Min; Kim, Hyunkyung; Nam, Hye Jin; Shin, Hi-Jai R.; Kim, Dongha; Ko, Enyoung; Noh, Dong-Young; Kim, Keun Il; Kim, Jung Hwa; Baek, Sung Hee
- Issue Date
- Sep-2010
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Bcl3; CtBP1; Apoptosis; Cancer; Ubiquitination
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.400, no.3, pp 396 - 402
- Pages
- 7
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 400
- Number
- 3
- Start Page
- 396
- End Page
- 402
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13125
- DOI
- 10.1016/j.bbrc.2010.08.084
- ISSN
- 0006-291X
1090-2104
- 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 (C) 2010 Elsevier Inc All rights reserved
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