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Nucleic Acids Research Advance Access published online on June 27, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn417
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Nuclear epidermal growth factor receptor (EGFR) interacts with signal transducer and activator of transcription 5 (STAT5) in activating Aurora-A gene expression

Liang-Yi Hung1,2,3,*, Joseph T. Tseng1,2,4, Yi-Chao Lee1,2, Weiya Xia5, Ying-Nai Wang5, Min-Li Wu1,2, Yu-Hsuan Chuang1,2, Chein-Hsien Lai1 and Wen-Chang Chang1,2,3

1Department of Pharmacology, College of Medicine, 2Center for Gene Regulation and Signal Transduction Research, 3Institute of Biosignal Transduction, 4Institute of Bioinformatics, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 70101, Taiwan and 5Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA

*To whom correspondence should be addressed: Tel: +886 6 2080100; Fax: +886 6 2083663; Email: lyhung{at}mail.ncku.edu.tw Correspondence may also be addressed to Wen-Chang Chang; Email: wcchang{at}mail.ncku.edu.tw

Received December 12, 2007. Revised June 14, 2008. Accepted June 16, 2008.

Loss of the maintenance of genetic material is a critical step leading to tumorigenesis. It was reported that overexpression of Aurora-A and the constitutive activation of the epidermal growth factor (EGF) receptor (EGFR) are implicated in chromosome instability. In this study, we examined that when cells treated with EGF result in centrosome amplification and microtubule disorder, which are critical for genetic instability. Interestingly, the expression of Aurora-A was also increased by EGF stimulus. An immunofluorescence assay indicated that EGF can induce the nuclear translocation of EGFR. Chromatin immunoprecipitation (ChIP) and re-ChIP assays showed significant EGF-induced recruitment of nuclear EGFR and signal transducer and activator of transcription 5 (STAT5) to the Aurora-A promoter. A co-immunoprecipitation assay further demonstrated that EGF induces nuclear interaction between EGFR and STAT5. A small interfering (si)RNA knockdown assay also showed that EGFR and STAT5 are indeed involved in EGF-increased Aurora-A gene expression. Altogether, this study proposes that the nuclear EGFR associates with STAT5 to bind and increase Aurora-A gene expression, which ultimately may lead to chromosome instability and tumorigenesis. The results also provide a novel linkage between the EGFR signaling pathway and overexpression of Aurora-A in tumorigenesis and chromosome instability.

The authors wish it to be known that, in their opinion, the second and third authors should be regarded as joint Second Authors


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