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nonmetastatic melanoma cells die rapidly after they are introduced into the circulation, whereas many metastatic cells survive (3, 4). Subsequent studies concluded that nonmetastatic cells exhibited high levels ofiNOS activity and NO, whereas metastatic cells did not, thus demonstrating an inverse correlation between production of endogenous NO and the ability of K-1735 cells to survive in syngeneic mice to produce lung metastases (28). The purpose of this study was to provide evidence of a causal relation between enhanced iNOS activity in tumor cells and decreased metastatic potential. Q. W. Xie et al. have recently reported the cloning and characterization of iNOS cDNAs from mouse macrophages (29) that encoded two isoforms of iNOS. The enzymaticaUy active piNOS-L8 has a longer coding region and the other, enzymatically inactive piNOS-S2 has a shorter coding region differing at the COOH terminus (30). The inactivity of piNOS-S2 has been attributed to its inability to bind NADPH (30). In this study, we transfected these iNOS genes into highly metastatic iNOSdeficient K-1735 C4 melanoma cells. Transfection with cDNA encoding-active iNOS induces apoptosis, suppresses tumor growth, and abrogates production of metastasis

Year: 1995
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