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Inhibition of Experimental Metastasis by an -Glucosidase Inhibitor, 1,6-Epi-cyclophellitol

Institute of Microbial Chemistry, 3-14-23 Kamiosaki, Shinagawa-ku, Tokyo 141 [S. A., C. N., H. I.], and Department of Applied Chemistry, Faculty of Science and Technology, Keio University, 3-14-1 Hiyoshi, Kohoku-ku, Yokohama 223 [Y. O., K. U.], Japan

Isolated from a culture filtrate of Phellinus sp., cyclophellitol is a specific inhibitor of ß-glucosidase, but unlike castanospermine, it does not inhibit experimental metastasis. However, its structural analogue, 1,6-epicyclophellitol, inhibited -glucosidase as well as ß-glucosidase, and inhibited experimental metastasis. 1,6-Epi-cyclophellitol depressed -glucosidase activity in cultured B16/F10 cells after 48 h of incubation. Preincubation of B16/F10 cells for 48 h with 1,6-epi-cyclophellitol inhibited invasion of the cells in a Boyden chamber assay at the doses effective in inhibiting -glucosidase in situ. Pulmonary metastasis of B16/F10 cells in mice was inhibited by pretreatment of the cells with 1,6-epicyclophellitol in culture. The inhibitor reduced the collagen type I- and IV-mediated attachment of the cells, whereas it had no effect on laminin-mediated attachment. These results suggest that -glucosidase in tumor cells is essential for the metastatic process through the cellular interaction with collagen type I and IV.

¹ To whom requests for reprints should be addressed.

Received 3/31/93. Accepted 8/ 9/93.

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