Effects of hepatocyte growth factor on E-cadherin-mediated cell-cell adhesion in DU145 prostate cancer cells

Objectives. To examine how hepatocyte growth factor (HGF) affects cell-cell adhesion junctions on scattering in prostate cancer cells. HGF is known to induce scattering (dispersion of clustered cells into single cells) in various epithelial cells, including prostate cancer cells, but the mechanisms...

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Veröffentlicht in:Urology (Ridgewood, N.J.) N.J.), 2001-12, Vol.58 (6), p.1064-1069
Hauptverfasser: Miura, Hidenobu, Nishimura, Kenji, Tsujimura, Akira, Matsumiya, Kiyomi, Matsumoto, Kunio, Nakamura, Toshikazu, Okuyama, Akihiko
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Sprache:eng
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Zusammenfassung:Objectives. To examine how hepatocyte growth factor (HGF) affects cell-cell adhesion junctions on scattering in prostate cancer cells. HGF is known to induce scattering (dispersion of clustered cells into single cells) in various epithelial cells, including prostate cancer cells, but the mechanisms surrounding this action are not fully understood. Cell-cell adhesion junctions are composed of E-cadherin and its associated intracellular catenins and play important roles in the maintenance of cell integrity. Methods. The human prostate cancer cell line DU145 was used in this study. The associations and changes of various adhesion molecules with HGF treatment were investigated by inhibition assays, Western blot analysis, and immunofluorescence staining. Results. In the inhibition assay, anti-E-cadherin neutralizing monoclonal antibody caused the dissociation of DU145 cells similar to the scattering with HGF treatment. The expression of E-cadherin decreased with HGF, and the expression of alpha-catenin and beta-catenin did not change by Western blot analysis. In immunofluorescence staining, HGF caused the translocation of E-cadherin from cell-cell adhesion junctions to the cytoplasm. Conclusions. These results indicate that HGF induces scattering by decreasing the expression of E-cadherin and causes its translocation to the cytoplasm of DU145 cells.
ISSN:0090-4295
1527-9995
DOI:10.1016/S0090-4295(01)01427-3