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Ganglioside  GD 3 is highly expressed in human melanomas and enhances malignant properties of melanomas, such as cell proliferation and invasion activity. In this study, we analyzed the effects of  GD 3 expression on cell signals triggered by hepatocyte growth factor ( HGF )/Met interaction and by adhesion to collagen type I ( CL ‐I). Although stimulation of melanoma N1 cells ( GD 3+ and  GD 3−) with either  HGF  or adhesion to  CL ‐I did not show marked differences in the phosphorylation levels of Akt at Ser473 and Thr308 between two types of cells, simultaneous treatment resulted in definite and markedly increased activation of Akt in  GD 3+ cells. Similar increases were also shown in Erk1/2 phosphorylation levels with the costimulation in  GD 3+ cells. When resistance to induced apoptosis by H 2 O 2  was examined, only  GD 3+ cells treated with both  HGF  and adhesion to  CL ‐I showed clearly low percentages of dead cells compared with  GD 3− cells or  GD 3+ cells treated with either one of the stimulants. Cell growth measured by 5‐ethynyl‐2‘ deoxyuridine uptake also showed synergistic effects in  GD 3+ cells. These results suggested that  GD 3 plays a crucial role in the convergence of multiple signals, leading to the synergistic effects of those signals on malignant properties of melanomas.

Ganglioside GD 3 induces convergence and synergism of adhesion and hepatocyte growth factor/Met signals in melanomas