Abstract
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.
Highlights
Our 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
Since interferon regulatory factor binding protein (IBP) is correlated with the malignant behaviour of human breast cancer cells [16] and is down-regulated by p53 and DNA damaging agent in MCF-7 cells, we explored the importance of IBP in the response of MCF-7 to cisplatin
We found that IBP promotes the proliferation and migration of breast cancer cells and its expression is negatively correlated with p53 levels [16]
Summary
Our 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. Among the roles of p53, its tumor-suppression activity is associated with its ability to function as a transcriptional master regulator [2]. The identification of additional p53 target genes is steadily progressing and may elucidate the mechanisms by which p53 exerts its tumour-suppression activity. Breast cancer is the most frequent cancer in women. An estimated 1.15 million new cases of breast cancer were identified in 2002. In China, breast cancer registries record annual incidence increases of 3% to 4% [3]. Genetic studies have revealed that at least one third of nonfamilial breast cancers contain mutations in p53 [4], and
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