Amplification and Overexpression ofCTTN(EMS1) Contribute to the Metastasis of Esophageal Squamous Cell Carcinoma by Promoting Cell Migration and Anoikis Resistance
| Autor: | Xiao-Ming Shen, Ming-Rong Wang, Man-Li Luo, Xun Zhang, Yu Zhang, Fang Wei, Min Wu, Yan Cai, Xin Xu, Qimin Zhan, Yuntian Sun |
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| Rok vydání: | 2006 |
| Předmět: |
Cancer Research
Esophageal Neoplasms Cell Biology Metastasis Cell Movement medicine Humans Gene silencing Anoikis RNA Neoplasm Neoplasm Metastasis In Situ Hybridization Fluorescence PI3K/AKT/mTOR pathway DNA Primers Oligonucleotide Array Sequence Analysis Regulation of gene expression Oncogene Reverse Transcriptase Polymerase Chain Reaction Chromosomes Human Pair 11 Gene Amplification Chromosome Mapping Cell migration medicine.disease Gene Expression Regulation Neoplastic medicine.anatomical_structure Oncology Carcinoma Squamous Cell Cancer research Cortactin |
| Zdroj: | Cancer Research. 66:11690-11699 |
| ISSN: | 1538-7445 0008-5472 |
| Popis: | 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) |
| Databáze: | OpenAIRE |
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