This Article Full Text Full Text (PDF) Supplementary Data Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Luo, M.-L. Articles by Wang, M.-R. Search for Related Content PubMed PubMed Citation Articles by Luo, M.-L. Articles by Wang, M.-R.

Amplification and Overexpression of CTTN (EMS1) Contribute to the Metastasis of Esophageal Squamous Cell Carcinoma by Promoting Cell Migration and Anoikis Resistance

¹ State Key Laboratory of Molecular Oncology and ² Department of Pathology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China

Requests for reprints: Ming-Rong Wang, State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, P.O. Box 2258, Beijing 100021, China. Phone: 86-10-87788204; Fax: 86-10-87778651; E-mail: wangmr04{at}126.com.

Gain of chromosome 11q13 is a common event in esophageal squamous cell carcinoma (ESCC). The cortactin gene (CTTN, also EMS1), located at 11q13, plays a pivotal role in coupling membrane dynamics to cortical actin assembly. This gene has been implicated in the motility of several types of cells. In the present study, we found that the amplification and overexpression of the CTTN gene was associated with lymph node metastasis in ESCC. Functional analysis by small interfering RNA–mediated silencing of CTTN revealed that in addition to the effect on cell migration, CTTN influenced cell invasiveness by anoikis resistance. In vivo assay showed that inhibition of CTTN expression also decreased tumor growth and lung metastasis of ESCC cells. At the molecular level, we showed for the first time that the protective role of CTTN in anoikis resistance was correlated with the activation of the phosphatidylinositol 3-kinase/Akt pathway. Overall, the data suggest that CTTN is an oncogene in the 11q13 amplicon and exerts functions on tumor metastasis in ESCC. (Cancer Res 2006; 66(24): 11690-9)

This article has been cited by other articles:

				Y.-S. Lee, K.-H. Lim, X. Guo, Y. Kawaguchi, Y. Gao, T. Barrientos, P. Ordentlich, X.-F. Wang, C. M. Counter, and T.-P. Yao The Cytoplasmic Deacetylase HDAC6 Is Required for Efficient Oncogenic Tumorigenesis Cancer Res., September 15, 2008; 68(18): 7561 - 7569. [Abstract] [Full Text] [PDF]

				J. H. Gibcus, L. Menkema, M. F. Mastik, M. A. Hermsen, G. H. de Bock, M.-L. F. van Velthuysen, R. P. Takes, K. Kok, C. A. Alvarez Marcos, B. F.A.M. van der Laan, et al. Amplicon Mapping and Expression Profiling Identify the Fas-Associated Death Domain Gene as a New Driver in the 11q13.3 Amplicon in Laryngeal/Pharyngeal Cancer Clin. Cancer Res., November 1, 2007; 13(21): 6257 - 6266. [Abstract] [Full Text] [PDF]

				P. Timpson, A. S. Wilson, G. M. Lehrbach, R. L. Sutherland, E. A. Musgrove, and R. J. Daly Aberrant Expression of Cortactin in Head and Neck Squamous Cell Carcinoma Cells Is Associated with Enhanced Cell Proliferation and Resistance to the Epidermal Growth Factor Receptor Inhibitor Gefitinib Cancer Res., October 1, 2007; 67(19): 9304 - 9314. [Abstract] [Full Text] [PDF]

				W.-C. Tsai, J.-S. Jin, W.-K. Chang, D.-C. Chan, M.-K. Yeh, S.-C. Cherng, L.-F. Lin, L.-F. Sheu, and Y.-C. Chao Association of Cortactin and Fascin-1 Expression in Gastric Adenocarcinoma: Correlation With Clinicopathological Parameters J. Histochem. Cytochem., September 1, 2007; 55(9): 955 - 962. [Abstract] [Full Text] [PDF]