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Hirao, T. et al.

Overexpression of ADAM9 enhances growth factor- mediated recycling of E-cadherin in human colon cancer cell line HT29 cells.

Growth factor-mediated stimulation of epithelial cells induces the disassembly of E-cadherin-mediated cell-cell adhesion. We found that overexpression of a disintegrin and metalloprotease 9 (ADAM9) enhanced growth factor- mediated induction of endocytosis and dynamic recycling of E-cadherin in HT29 human colon cancer cells. In addition, ubiquitination and degradation of E-cadherin were reduced in these cells. ADAM9 constitutively interacted with E-cadherin, and the two proteins co-localized at the plasma membrane of HT29 cells. Administration of a metalloprotease inhibitor or overexpression of an ADAM9 mutant lacking metalloprotease activity attenuated growth factor-dependent endocytosis and recycling of E-cadherin as well as scattering of HT29 cells. These results suggest that the metalloprotease activity of ADAM9 mediates growth factor- induced endocytosis and dynamic recycling of E-cadherin and prevents E-cadherin degradation.[1]

References

Overexpression of ADAM9 enhances growth factor-mediated recycling of E-cadherin in human colon cancer cell line HT29 cells. Hirao, T., Nanba, D., Tanaka, M., Ishiguro, H., Kinugasa, Y., Doki, Y., Yano, M., Matsuura, N., Monden, M., Higashiyama, S. Exp. Cell Res. (2006) [Pubmed]

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