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Abstract
Abstract PURPOSE: Epithelial-mesenchymal transition (EMT) is a process by which cancer cells acquire mesenchymal properties, such as induction of N-cadherin, while epithelial-associated genes like E-cadherin are lost. This enables the cells to be more invasive, migratory and metastatic. Factors that can induce EMT include growth factors like transforming growth factor -β (TGF-β) and epidermal growth factor (EGF), and transcription factors like Snail1. Snail1-induced EMT promotes migration and invasion and we hypothesized that this may be mediated by urokinase (uPA) and its receptor (uPAR) activities. uPA, a serine protease, may be activated by integrin engagement to bind to its receptor, uPAR, and initiate a signaling cascade that regulates a variety of biological pathways including migration and invasion. DESIGN METHODS: 22Rv1, LNCaP and ARCaP human prostate cancer (PC) cells were stably transfected with empty vector control (Neo) or constitutively active Snail which led to increased cell migration and invasion. The levels of Snail, uPA, and uPAR were measured by Western Blot analysis. uPA activity in conditioned media was measured using the Elisa uPA activity assay kit. Also, cells were treated with PI3K and MAPK inhibitors at set time points. RESULTS: The data suggests that overexpression of Snail1 increased uPA and uPAR protein levels, while uPA activity was elevated in conditioned media from ARCaP, LNCaP and 22Rv1 cells transfected with Snail. In addition, MAPK inhibitor, UO126, inhibited ERK activity within 30 min up to 72 h, and decreased uPA activity within 24 h. CONCLUSION: Therefore, Snail-mediated cell migration and invasion in human prostate cancer cells may occur via the regulation of uPA/uPAR and MAPK activities. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3430. doi:10.1158/1538-7445.AM2011-3430
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