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Correlation between E-Cadherin Expression and Invasiveness in Vitro in a Human Esophageal Cancer Cell Line¹

Department of Surgery II, Osaka University Medical School, 1-1-50 Fukushima, Fukushima-ku, Osaka 553, Japan [Y. D., H. S., H. T., M. I., H. O., K. I., T. K., T. M.], and Department of Biophysics, Faculty of Science, Kyoto University, Kitashirakawa, Sakyo-ku, Kyoto 606, Japan [M. T.]

E-cadherin, a member of the cadherin family, plays a major role in cell-cell adhesion of normal epithelium. Recent studies have shown that reduction or loss of E-cadherin expression in carcinomas have some relationship with their clinicopathological manifestation including invasion and metastasis. In the present study, we have established cell clones with different E-cadherin expression from human esophageal cancer, TE-2, and examined their adhesive capacity and invasiveness in vitro. Cell clones with positive E-cadherin expression [ECD(+) cells] were round and formed cobblestone colonies, while cell clones negative for E-cadherin [ECD(-) cells] had spindle shapes and formed dispersed colonies. ECD(+) cells showed higher adhesive capacity than ECD(-) cells, in both an aggregation assay with gyratory shaking culture and a dissociation assay of cells passing through the micropore membrane. Monoclonal antibody against human E-cadherin (HECD1) effectively diminished the mutual adhesion of ECD(+) cells but did not affect that of ECD(-) cells. Tumor invasiveness was evaluated with organotypic raft culture which is a coculture system consisting of two layers, a collagen gel layer containing fibroblasts and overlying reconstituted stratified squamous epithelium. ECD(+) cells formed complete stratified epithelium, but ECD(-) cells did not. ECD(+) cells did not invade the collagen/fibroblast gel, but ECD(-) cells did. Furthermore, ECD(+) cells showed invasion when an antibody against E-cadherin was used. Thus, loss or dysfunction of E-cadherin diminishes intercellular adhesion and results in the acquisition of invasive capacity in the cell line we examined.

¹ Supported in part by Grant-in-Aid for cancer research (No. 04454333) from the Ministry of Education, Science, and Culture, Japan.

² To whom requests for reprints should addressed.

Received 3/ 4/93. Accepted 5/10/93.

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