Interferon regulatory factor 4 binding protein is a novel p53 target gene and suppresses cisplatin-induced apoptosis of breast cancer cells

Molecular Cancer

Research

Fang Yuan¹  Chuanmin Hu²  Peng Li²  Mingzhen Yang²  An Chen²  Shuhui Li²  Zhongjiao Chen² 

[1] Department of Cell Biology, Third Military Medical University, 400038, Chongqing, P.R. China;Urology Institute of People’s Liberation Army, Southwest Hospital, Third Military Medical University, 400038, Chongqing, P.R. China;Department of Clinical Biochemistry, Third Military Medical University, 400038, Chongqing, P.R. China;

关键词: Breast cancer;    Interferon regulatory factor 4 binding protein (IBP);    p53;    Cisplatin;    Apoptosis;   

DOI  :  10.1186/1476-4598-11-54

 received in 2012-04-05, accepted in 2012-08-02,  发布年份 2012

来源: Springer

【 摘 要 】

BackgroundOur previous work demonstrated that ectopic expression of interferon regulatory factor 4 binding protein (IBP) was correlated with the malignant behaviour of human breast cancer cells. The mechanisms controlling differential expression of IBP in breast cancer still remain unknown.ResultsTo investigate the mechanism of IBP dysregulation in breast cancer, we identified IBP was a novel p53 target gene. IBP expression was negatively regulated by wild-type p53 and was p53 dependently suppressed by DNA damage agent cisplatin. Furthermore, high levels of IBP were found to decrease cisplatin-induced growth suppression and apoptotic cell death, which was associated with decreased p53 activity and imbalanced Bcl-2 family member expression.ConclusionsIBP is a novel p53 target gene which suppresses cisplatin-mediated apoptosis of breast cancer cells via negative feedback regulation of the p53 signalling pathway, suggesting IBP may serve as a target for pharmacologic intervention of breast cancer resistant to cisplatin therapy.

【 授权许可】

Unknown   
© Yang et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.