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• W2037668836 abstract "c-Met is a transmembrane tyrosine kinase receptor that may be activated by hepatocyte growth factor, an inducer of epithelial-mesenchymal transition (EMT), to regulate the associated downstream gene expression. This process is critical to cell migration in normal and pathological conditions. In the present study, the function of c-Met in the process of EMT was investigated in prostate cancer. Initially, a c-Met stable expression cell line was constructed using EMT- and c-Met-negative LNCaP prostate cancer cells. Following the identification of c-Met in the transfected cells, the changes in EMT, phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated kinase pathway biomarkers were determined by western blot analysis. MTT, soft agar and Transwell assays, and xenograft studies were used to investigate the effects of c-Met on the proliferation, migration and tumorigenicity of LNCaP cells. The results of the present study revealed downregulation of E-cadherin and upregulation of vimentin in LNCaP-Met cells. The results demonstrated that c-Met enhanced proliferation, migration and tumorigenicity capacity when compared with LNCaP and LNCaP-pcDNA3.1 cells. Furthermore, these EMT-like changes were mediated via the PI3K and mitogen-activated protein kinase signaling pathways. The present study clearly demonstrates a crucial function for c-Met in EMT development in prostate cancer. c-Met-targeted treatment may be an effective adjuvant therapy for improving survival rates in patients with prostate cancer." @default.
• W2037668836 created "2016-06-24" @default.
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• W2037668836 date "2014-07-28" @default.
• W2037668836 modified "2023-10-10" @default.
• W2037668836 title "Overexpression of c-Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo" @default.
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• W2037668836 doi "https://doi.org/10.3892/ol.2014.2390" @default.
• W2037668836 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4156182" @default.
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• W2037668836 hasPublicationYear "2014" @default.
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