Abstract 2399: Syntenin-1 promotes cell invasion though regulating Slug-dependent epithelial-mensenchymal transition in non-small cell lung cancer

Abstract

Abstract Slug, a transcriptional repressor, is involved in the regulation of epithelial-mesenchymal transition (EMT) during development and can promote cancer cell invasion and metastasis. Through Yeast-two hybrid screening, we found that syntenin-1, a tandem PDZ protein, can associate with Slug. Syntenin-1 is known to involve in many biological functions such as protein traffics and cytoskeleton remodeling. Recently, it has been found that overexpression of syntenin-1 may promote cancer cell invasion by altering defined biochemical and signaling pathways, including c-Src/ focal adhesion kinase (FAK) and NF-kappaB. Conversely, knock-down the expression of syntenin-1 can also increase cell aggregation. All these findings indicate that syntenin-1 may play an important role in cell adhesion and movement. Whether syntenin-1 is involved in the process of EMT should be further clarified. In this study, we showed that syntenin-1 could enhance Slug-dependent cell invasion and regulate the EMT in lung cancer cells. Syntenin-1 can interact with Slug through its PDZ-1 domain and increase their nuclear localization in cells. Overexpression of syntenin-1 increases Slug-induced cell migration and invasion though regulating the repression activity of Slug. Knock down the expression of syntenin-1 may also inhibit the repression activity of Slug on promoter of E-cadherin in highly invasive lung cancer cell lines. In Sum, Syntenin-1 may promote cell Invasion though regulating Slug-dependent EMT process in Non-small cell lung cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2399. doi:1538-7445.AM2012-2399