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

Abstract	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.
Authors	Takafumi Hirao, Daisuke Nanba, Motonari Tanaka, Hiroshi Ishiguro, Yumi Kinugasa, Yuichiro Doki, Masahiko Yano, Nariaki Matsuura, Morito Monden, Shigeki Higashiyama
Journal	Experimental cell research (Exp Cell Res) Vol. 312 Issue 3 Pg. 331-9 (Feb 01 2006) ISSN: 0014-4827 [Print] United States
PMID	16336960 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Cadherins HBEGF protein, human Heparin-binding EGF-like Growth Factor Intercellular Signaling Peptides and Proteins Membrane Proteins Ubiquitin Epidermal Growth Factor Metalloproteases ADAM Proteins ADAM9 protein, human
Topics	ADAM Proteins (genetics, metabolism) Cadherins (metabolism) Colonic Neoplasms (drug therapy, metabolism, pathology) Endocytosis Epidermal Growth Factor (pharmacology) HT29 Cells Heparin-binding EGF-like Growth Factor Humans Intercellular Signaling Peptides and Proteins Membrane Proteins (genetics, metabolism) Metalloproteases (metabolism) Mutation Ubiquitin (metabolism) Up-Regulation

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