Abstract

Abstract Identification of a molecular signature associated with epithelial to mesenchymal transition (EMT) may provide insight into the potential of a tumor to metastasize. To this effect we have undertaken a systems approach to understanding EMT with transcript and proteomic profiling of 30 lung adenocarcinoma cell lines. In-depth proteomic profiling was performed on conditioned media, cell surface and whole cell lysates from lung adenocarcinoma cell lines, allowing characterization as epithelial or mesenchymal based on their levels of E-cadherin and Vimentin, as well as cell morphology. Gene and protein expression from five cell lines that exhibited mesenchymal features were compared with five cell lines that exhibited epithelial features to identify proteins specifically associated with either a mesenchymal or epithelial phenotype. We identified protein signatures specific for mesenchymal or epithelial cells in the whole cell lysates, cell surface and conditioned media, with secreted proteins in the conditioned media representing the most distinct signature based on cluster analysis of protein expression. A much larger number of proteins were specific for epithelial cells than for mesenchymal, suggesting tighter regulation of expression in the epithelial cells. Networks of proteins associated with cell motion, extracellular matrix and growth regulation were identified that were distinct for mesenchymal cell lines while epithelial cell lines exhibited networks of proteins associated with metabolism and cell adhesion. Gene expression analysis of these cell lines supports the observations of tighter gene regulation in epithelial cells as well as the identified protein networks. Identification of a protein signature for EMT provides further understanding of a critical step in tumor progression and has the potential to yield biomarkers to assess likelihood of tumor metastasis in lung adenocarcinoma. 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 3426. doi:10.1158/1538-7445.AM2011-3426

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