Plant-glycoside modulation of cell surface related to control of differentiation in cultured B16 melanoma cells.

Abstract

We have shown that the ginsenosides Rh1 and Rh2, which are plant glycosides with a dammarane skeleton resembling a steroid skeleton as an aglycone, control the phenotypic expression of mouse B16 melanoma cells in different ways. The effects of Rh1 and Rh2 on the cell surface were studied to clarify the relationship between the control of phenotypic expression and modification of the cell surface in B16 melanoma cells. Rh2, which has the capacity to inhibit the growth of and to stimulate melanogenesis in B16 melanoma cells, causes flattening of the cells cultured in a collagen gel, leading to organized, nonoverlapping monolayers. Cell-to-cell adhesiveness and cell-to-substrate adhesiveness were markedly increased in the B16 melanoma cells treated with Rh2. In Rh2-treated cells, the binding of peanut agglutinin on the cell surface was also increased, whereas no marked changes were observed in the binding of concanavalin A or wheat germ agglutinin. In contrast, Rh1, which showed no effect on cell growth, but did stimulate melanogenesis, did not cause morphological changes of the cells and exerted no effect on cell adhesiveness or cell surface lectin binding. 1,6-Diphenyl-1,3,5-hexatriene polarization values markedly decreased in cells treated with either Rh1 or Rh2. Rh2 was found to be incorporated in the lipid fraction of the B16 melanoma cell membrane. In contrast, Rh1 was not detected in the lipid fraction of B16 melanoma cells. However, novel lipid components were found.