Bcl3-dependent stabilization of CtBP1 is crucial for the inhibition of apoptosis and tumor progression in breast cancer

Hee June Choi, Ji Min Lee, Hyunkyung Kim, Hye Jin Nam, Hi Jai R. Shin, Dongha Kim, Enyoung Ko, Dong Young Noh, Keun Il Kim, Jung Hwa Kim, Sung Hee Baek

Research output: Contribution to journalArticlepeer-review

34 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)396-402
Number of pages7
JournalBiochemical and biophysical research communications
Issue number3
Publication statusPublished - 2010 Sept
Externally publishedYes


  • Apoptosis
  • Bcl3
  • Cancer
  • CtBP1
  • Ubiquitination

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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