Noto Y, Iwazaki A, Nagao J, Sumiyama Y, Redpath J L, Stanbridge E J, Kitagawa T
Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Tokyo, Japan.
Biochem Biophys Res Commun. 1997 Nov 17;240(2):395-8. doi: 10.1006/bbrc.1997.7650.
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 expresses a larger glucose transporter, GLUT1, due to altered glycosylation when compared to the nontumorigenic counterpart CGL1. In this study, we demonstrated this glycosylation change in GLUT1 in gamma-ray-induced tumorigenic mutants (GIMs) isolated from CGL1 cells as expressing a tumor-associated surface antigen, intestinal alkaline phosphatase. In contrast, GLUT1 in the gamma-irradiated nontumorigenic control cells (CONs) did not show this alteration. In accordance with this glycosylation change, affinity to 2-deoxyglucose in these GIM clones was increased by about twofold when compared to the nontumorigenic CONs. These results suggest a close correlation between the glycosylation change in GLUT1 with increased affinity to D-glucose and tumorigenicity of these human cell hybrids.
对子宫颈癌细胞系海拉细胞（HeLa）与正常成纤维细胞之间的人细胞杂种进行的研究表明，它们的致瘤性受11号染色体上一种假定的肿瘤抑制基因控制。我们之前已经证明，与非致瘤性对应物CGL1相比，致瘤性细胞杂种CGL4由于糖基化改变而表达一种更大的葡萄糖转运蛋白GLUT1。在本研究中，我们在从CGL1细胞分离出的γ射线诱导的致瘤突变体（GIMs）中证明了GLUT1的这种糖基化变化，这些突变体表达一种肿瘤相关表面抗原——肠碱性磷酸酶。相比之下，γ射线照射的非致瘤性对照细胞（CONs）中的GLUT1未显示这种改变。与这种糖基化变化一致，与非致瘤性CONs相比，这些GIM克隆对2-脱氧葡萄糖的亲和力增加了约两倍。这些结果表明GLUT1糖基化变化与对D-葡萄糖亲和力增加以及这些人细胞杂种的致瘤性之间存在密切关联。
