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Article

Overexpression of c‑Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo

  • Authors:
    • Yili Han
    • Yong Luo
    • Jiahui Zhao
    • Mingchuan Li
    • Yongguang Jiang
  • View Affiliations / Copyright

    Affiliations: Department of Urology, Beijing Anzhen Hospital Affiliated to Capital Medical University, Beijing 100029, P.R. China
  • Pages: 1618-1624
    |
    Published online on: July 28, 2014
       https://doi.org/10.3892/ol.2014.2390
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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.
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Copy and paste a formatted citation
Spandidos Publications style
Han Y, Luo Y, Zhao J, Li M and Jiang Y: Overexpression of c‑Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo. Oncol Lett 8: 1618-1624, 2014.
APA
Han, Y., Luo, Y., Zhao, J., Li, M., & Jiang, Y. (2014). Overexpression of c‑Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo. Oncology Letters, 8, 1618-1624. https://doi.org/10.3892/ol.2014.2390
MLA
Han, Y., Luo, Y., Zhao, J., Li, M., Jiang, Y."Overexpression of c‑Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo". Oncology Letters 8.4 (2014): 1618-1624.
Chicago
Han, Y., Luo, Y., Zhao, J., Li, M., Jiang, Y."Overexpression of c‑Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo". Oncology Letters 8, no. 4 (2014): 1618-1624. https://doi.org/10.3892/ol.2014.2390
Copy and paste a formatted citation
x
Spandidos Publications style
Han Y, Luo Y, Zhao J, Li M and Jiang Y: Overexpression of c‑Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo. Oncol Lett 8: 1618-1624, 2014.
APA
Han, Y., Luo, Y., Zhao, J., Li, M., & Jiang, Y. (2014). Overexpression of c‑Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo. Oncology Letters, 8, 1618-1624. https://doi.org/10.3892/ol.2014.2390
MLA
Han, Y., Luo, Y., Zhao, J., Li, M., Jiang, Y."Overexpression of c‑Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo". Oncology Letters 8.4 (2014): 1618-1624.
Chicago
Han, Y., Luo, Y., Zhao, J., Li, M., Jiang, Y."Overexpression of c‑Met increases the tumor invasion of human prostate LNCaP cancer cells in vitro and in vivo". Oncology Letters 8, no. 4 (2014): 1618-1624. https://doi.org/10.3892/ol.2014.2390
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