Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data of HGF/cMET pathway in prostate cancer DU145 cell line


ABSTRACT: DU145 prostate cancer cells were treated with 25 ng/ml hepatocyte growth factor (HGF) or vehicle for 2, 8, or 24 hours. HGF stimulates the cMET protein, a tyrosine kinase transmembrane protein. The aim of this study is to determine the role of the HGF/cMET pathway in immature cells of established prostate cancer. HGF stimulation of DU145 prostate cancer cell line led to cell migration in culture, formation of sprouts in Matrigel and inhibition of growth. These biological effects went together with induction of a stem-like phenotype as defined by up-regulation of CD49b, CD49f, CD44 and SOX9, and down-regulation of CD24 on gene-expression arrays and quantitative PCR. The shift towards a stem-like phenotype was reflected by protein modifications on FACS, Western blot, and enhanced rapid adhesion to collagen I. Small molecules SU11274 and PHA665752 were able to inhibit both morphologic and molecular HGF effects. DU145 cells were stimulated for 2, 8 and 24 hours with 25 ng/ml HGF or vehicle. For each time point two arrays analyses were performed. One for cells stimulated with a vehicle and one for the HGF stimulated cells. Six arrays were performed in total in this study.

ORGANISM(S): Homo sapiens

SUBMITTER: Guido Jenster 

PROVIDER: E-GEOD-16659 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


Prostate cancer consists of secretory cells and a population of immature cells. The function of immature cells and their mutual relation with secretory cells are still poorly understood. Immature cells either have a hierarchical relation to secretory cells (stem cell model) or represent an inducible population emerging upon appropriate stimulation of differentiated cells. Hepatocyte Growth Factor (HGF) receptor c-MET is specifically expressed in immature prostate cells. Our objective is to deter  ...[more]

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