ALTERED N-GLYCOSYLATION OF GLUCOSE-TRANSPORTER-1 ASSOCIATED WITH RADIATION-INDUCED TUMORIGENESIS OF HUMAN CELL HYBRIDS

Studies on human cell hybrids between a cervical carcinoma cell line, HeLa, and normal fibroblasts have indicated that their tumorigenicity is under the control of a putative tumor suppressor on chromosome 11. We have previously demonstrated that a tumorigenic cell. hybrid CGL4 e xpresses a larger glucose transporter, GLUT1, due to altered glycosyla tion when compared to the nontumorigenic counterpart CGL1. In this stu dy, we demonstrated this glycosylation change in GLUT1 in gamma-ray-in duced tumorigenic mutants (GIMs) isolated from CGL1 cells as expressin g a tumor-associated surface antigen, intestinal alkaline phosphatase. In contrast, GLUT1 in the gamma-irradiated nontumorigenic control cel ls (CONs) did not show this alteration, In accordance with this glycos ylation change, affinity to a-deoxyglucose in these GIM clones was in creased by about twofold when compared to the nontumorigenic CONs, The se results suggest a close correlation between the glycosylation chang e in GLUT1 with increased affinity to D-glucose and tumorigenicity of these human cell hybrids. (C) 1997 Academic Press.