Oncogenic H-Ras reprograms madin-darby canine kidney (MDCK) cell-derived exosomal proteins following epithelial-mesenchymal transition

BJ Tauro; RA Mathias; DW Greening; SK Gopal; H Ji; EA Kapp; BM Coleman; AF Hill; U Kusebauch; JL Hallows; D Shteynberg; RL Moritz; HJ Zhu; RJ Simpson

Journal article

Oncogenic H-Ras reprograms madin-darby canine kidney (MDCK) cell-derived exosomal proteins following epithelial-mesenchymal transition

BJ Tauro, RA Mathias, DW Greening, SK Gopal, H Ji, EA Kapp, BM Coleman, AF Hill, U Kusebauch, JL Hallows, D Shteynberg, RL Moritz, HJ Zhu, RJ Simpson

Molecular and Cellular Proteomics | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC | Published : 2013

DOI: 10.1074/mcp.M112.027086

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Abstract

Epithelial-mesenchymal transition (EMT) is a highly conserved morphogenic process defined by the loss of epithelial characteristics and the acquisition of a mesenchymal phenotype. EMT is associated with increased aggressiveness, invasiveness, and metastatic potential in carcinoma cells. To assess the contribution of extracellular vesicles following EMT, we conducted a proteomic analysis of exosomes released from Madin-Darby canine kidney (MDCK) cells, and MDCK cells transformed with oncogenic H-Ras (21D1 cells). Exosomes are 40-100 nm membranous vesicles originating from the inward budding of late endosomes and multivesicular bodies and are released from cells on fusion of multivesicular bod..

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University of Melbourne Researchers

David Greening Author

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Grants

Awarded by National Human Genome Research Institute

Funding Acknowledgements

This work was supported by the National Health & Medical Research Council (NHMRC) of Australia for program grant #487922 (RJS, JH, DWG), grants #280913 and #433619 (H-JZ), grants #628946 and #400202 (AFH). AFH is also supported by an Australian Research Council (www.arc.gov.au) Future Fellowship (FT100100560). RAM is supported by an Early Career CJ Martin Fellowship #APP1037043, and BMC by an NHMRC Dora Lush Biomedical Postgraduate Scholarship #628959. BJT is supported by The University of Melbourne Research Scholarship. Analysis of proteomic data described in this work was supported using the Australian Proteomics Computational Facility funded by the National Health & Medical Research Council of Australia grant #381413. Electron microscopy was performed at the Advanced Microscopy Facility at the Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne. This work was also supported, in part, by American Recovery and Reinvestment Act funds through National Institutes of Health Grant R01 HG005805 (RLM), the NIGMS Grant 2P50 GM076547 from Center for Systems Biology, the Luxembourg Centre for Systems Biomedicine and the University of Luxembourg, and from the National Science Foundation (MRI Grant 0923536). UK was supported by a fellowship from the German Academic Exchange Service. We thank the NCI of the NIH for support (Grant #1R03CA156667 to RLM).