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A gene expression signature associated with K-Ras addiction reveals regulators of EMT and tumor cell survival

GSE15126 Homo sapiens Expression profiling by array; Genome binding/occupancy profiling by SNP array 60 samples Submitted 2009/03/06 Platform GPL1352Platform GPL3720Platform GPL3718
Summary
K-Ras mutations occur frequently in epithelial cancers. Using shRNAs to deplete K-Ras in lung and pancreatic cancer cell lines harboring K-Ras mutations, two classes were identified—lines that do or do not require K-Ras to maintain viability. Comparing these two classes of cancer cells revealed a gene expression signature in K-Ras-dependent cells, associated with a well-differentiated epithelial phenotype, which was also seen in primary tumors. Several of these genes encode pharmacologically tractable proteins, such as Syk and Ron kinases and integrin beta6, depletion of which induces epithelial-mesenchymal transformation (EMT) and apoptosis specifically in K-Ras-dependent cells. These findings indicate that epithelial differentiation and tumor cell viability are associated, and that EMT regulators in “K-Ras-addicted” cancers represent candidate therapeutic targets.
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Also filed as BioProject PRJNA114943. Searching any of these in the dataset finder brings you back here.

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