Regulation of lnvasive Potential of Human Prostate Cancer Cell Lines by Hepatocyte Growth Factor
Article first published online: 2 JUL 2007
International Journal of Urology
Volume 5, Issue 3, pages 276–281, May 1998
How to Cite
Nishimura, K., Kitamura, M., Takada, S., Nonomura, N., Tsujimura, A., Matsumiya, K., Miki, T., Matsumoto, K. and Okuyama, A. (1998), Regulation of lnvasive Potential of Human Prostate Cancer Cell Lines by Hepatocyte Growth Factor. International Journal of Urology, 5: 276–281. doi: 10.1111/j.1442-2042.1998.tb00603.x
- Issue published online: 2 JUL 2007
- Article first published online: 2 JUL 2007
- Received May 14,1997; accepted for publication in revised form Oct. 21, 1997
- hepatocyte growth factor;
- prostate cancer;
Background: The growth and progression of prostate cancer depends on the stromal-epithelial interaction which is under paracrine control. Hepatocyte growth factor (HGF), produced by mesenchymal cells, is a multifunctional growth factor stimulating the movement and growth of epithelial cells including cancer cells. We therefore assessed the relationship between the invasive potential of prostate cancer and HGF in vitro.
Methods: Three human prostate cancer cell lines were used including PC-3 and DU145 (androgenindependent), and LNCaP (androgen-dependent). We studied the expression of the HCF receptor c-met proto-oncogene (c-met) by Western blotanalysis, and alsodetermined theeffectsof HGF on cell scattering, and the mechanisms of invasion and proliferation, by microscopic observation, the matrigel invasion chamber assay, and the MTT assay.
Results: c-met was detected in PC-3 and DU145 cells, but not in the LNCaP cells. There was increased cell motility in the scatter assay and an increased cell invasive potential in the matrigel invasion chamber assay by stimulation with HGF only with DU145 cells.
Conclusion: HGF plays an important role in the invasion and metastasis of the DU145 cell line through a paracrine mechanism mediated by the c-metreceptor. In the PC-3 cell line, the lack of downstream signal transduction after the c-met receptor is suggested.