Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from rat tumors formed by 9L.EV or 9L.EGFRvIII cells

ABSTRACT: Analysis of rat tumor xenografts revealed genes that are upregulated in tumors expressing EGFRvIII 12 rats received intracranial injections of 9L cells expressing EGFRvIII or an empty vector control. Three weeks after implantation and subsequent growth, tumors were aseptically removed, processed for RNA extraction, and analyzed for gene expression profiling using the RatRef12 Illumina chip array. We compared the average expression of all the transcripts between EGFRvIII-expressing and empty vector control tumors.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Matthew Lazzara

PROVIDER: E-GEOD-51147 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Sprouty2 Drives Drug Resistance and Proliferation in Glioblastoma.

Walsh Alice M AM Kapoor Gurpreet S GS Buonato Janine M JM Mathew Lijoy K LK Bi Yingtao Y Davuluri Ramana V RV Martinez-Lage Maria M Simon M Celeste MC O'Rourke Donald M DM Lazzara Matthew J MJ

Molecular cancer research : MCR 20150501 8

<h4>Unlabelled</h4>Glioblastoma multiforme (GBM) is notoriously resistant to therapy, and the development of a durable cure will require the identification of broadly relevant regulators of GBM cell tumorigenicity and survival. Here, we identify Sprouty2 (SPRY2), a known regulator of receptor tyrosine kinases (RTK), as one such regulator. SPRY2 knockdown reduced proliferation and anchorage-independent growth in GBM cells and slowed xenograft tumor growth in mice. SPRY2 knockdown also promoted ce ...[more]

PMID: 25934697

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Project description:Glioblastoma multiforme (GBM) is a highly aggressive and heterogeneous form of primary brain tumors, driven by a complex repertoire of oncogenic alterations, including the constitutively active epidermal growth factor receptor (EGFRvIII). EGFRvIII impacts both cell-intrinsic and non-cell autonomous aspects of GBM progression, including cell invasion, angiogenesis and modulation of the tumor microenvoiront, this is, at least in part, attributable to the release and intercellular trafficking of extracellular vesicles (EVs), heterogeneous membrane structures containing multiple bioactive macromolecules. Here we analyzed the impact of EGFRvIII on the profile of glioma EVs using a series of isogenic tumor cell lines, in which this oncogene exhibits a strong transforming activity. Thus, we observed that EGFRvIII expression alters several properties of glioma EVs, including their output and global protein composition. Using mass spectrometry, quantitative proteomic analysis and Gene Ontology terms filters, we observed that EVs released by EGFRVIII-transformed cells were enriched for extracellular exosome and focal adhesion related proteins. Among them, we validated the association of pro-invasive proteins (CD44, BSG, CD151) with EVs of EGFRvIII expressing cells, and down-regulation of exosomal markers (CD81 and CD82) in EVs of their indolent counterparts. Nano-flow cytometry revealed that the EV output from individual glioma cell lines was highly heterogeneous, such that only a fraction of EVs contained specific proteins such as EGFR, CD9, or others. Notably, cells expressing EGFRvIII released ample EVs double positive for CD44/BSG, and these proteins also co-localized in cellular filopodia. We also detected the expression of homophilic adhesion molecules and increased homologous EV uptake by EGFRvIII-positive glioma cells. These results suggest that oncogenic EGFRvIII reprograms the proteome of GBM-related EVs, a notion with considerable implications for their biological activity and properties relevant for development of EV-based cancer biomarkers.

Dataset Information

Expression data from rat tumors formed by 9L.EV or 9L.EGFRvIII cells

Publications

Sprouty2 Drives Drug Resistance and Proliferation in Glioblastoma.

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