Abstract
Epithelial-Mesenchymal Transition (EMT) is a fundamental cellular process that occurs during embryonic development, wound healing, organ fibrosis and tumor invasion and metastasis. The molecular mechanism of EMT remains largely unknown; therefore, revealing the intricate mechanisms underlying EMT may help us to better understand how primary tumors become invasive and metastasize. The Madin-Darby canine kidney (MDCK) cell line is a polarized epithelial cell line that has been shown to be transformed into mesenchymal-like cells, when simultaneously stimulated by H-Ras and TGF- β. A hallmark of the early stage of EMT is the loss of cell polarity that occurs at the plasma membrane; moreover, a coordinated interaction of membrane proteins, such like transporters, linkers, receptors and enzyme, may play a crucial role in EMT progression. The main goal of this study is to develop a method for enriching membrane proteins and reducing proteomic complexity. Quantitative proteomic approaches will be used to compare the membrane proteome of modified MDCK cells in the early stage of EMT. Understanding of the molecular changes of the membrane proteome associated with EMT may help to provide a detailed insight into the mechanistic events underlying EMT.
Published Version
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