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Department of Biochemistry, Faculty of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113 [T. T., K. O., C. R., S. H.]; Department of Pure and Applied Science, College of Arts and Science, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153 [T. H., M. K.]; and Department of Biochemistry, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108 [E. T., A. K.], Japan
Glycolipid compositions of mouse mammary tumor cell FM3A and its Newcastle disease virus-resistant mutant cell, Had-1, which was also characterized as a defective mutant of UDP-galactose transport to Golgi apparatus, have been studied. The major neutral glycolipid in FM3A was Galß1-4Glcß1-1Cer (LacCer) (95%) and the rest was Glcß1-1Cer. The concentration of neutral glycolipids in Had-1 was only about one-fifth of that in FM3A. GlcB1-1Cer in Had-1 accounted for 79% of neutral glycolipids and the rest was LacCer, the content of which was decreased to 4% of that in FM3A. Ganglioside patterns of the two cell lines were similar, although gangliosides with N-glycolylneuraminic acid were increased in Had-1 cells compared with that in FM3A cells. The presence of NeuAc
2-3-Galß1-4GlcNAcß1-3Galß1-4Glcß1-1Cer, NeuAc
2-3Galß1-4GlcNAcß1-3Galß1-4GlcNAcß1-3Galß1-4Glcß1-2Cer, GM3, and GD3 was demonstrated by thin-layer chromatography immunostaining. 125I-Labeled Newcastle disease virus bound only poorly to gangliosides extracted from either FM3A or Had-1 cells on a high performance thin-layer chromatography plate. The effects of glycolipids on the growth of the two cell lines were also studied. Had-1 cells were more sensitive to glycolipids added exogenously than FM3A cells. Addition of GM3 had a stimulative effect on cell growth of Had-1. LacCer, Galß1-3GalNAcß1-4Galß1-4Glcß4-1Cer, and Glcß1-1Cer inhibited the growth of Had-1 cells. LacCer was the most potent inhibitor. LacCer immobilized on the culture plate also inhibited the growth of Had-1 cells. The inhibitory effect was recovered completely overcome by transferring the cells to LacCer-free medium. Had-1 cells were not tumorigenic in C3H/He mice, and furthermore the tumorigenic activity of FM3A cells was suppressed by the prior administration of Had-1 cells.
1 This work was supported in part by a Grant-in-Aid from the Ministry of Education, Science and Culture of Japan and from Nagase Science and Technology Foundation.
2 To whom requests for reprints should be addressed.
Received 8/13/90. Accepted 1/ 3/91.
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