AlteredN-Glycosylation of Glucose Transporter-1 Associated with Radiation-Induced Tumorigenesis of Human Cell Hybrids

1997 ◽  
Vol 240 (2) ◽  
pp. 395-398 ◽  
Author(s):  
Yasumitsu Noto ◽  
Ayano Iwazaki ◽  
Jiro Nagao ◽  
Yoshinobu Sumiyama ◽  
J.Leslie Redpath ◽  
...  
Keyword(s):  
Human Cell ◽  
Glucose Transporter ◽  
Glucose Transporter 1 ◽  
Cell Hybrids ◽  
Radiation Induced

Loss of Suppressor Loci on Chromosomes 11 and 14 May Be Required for Radiation-Induced Neoplastic Transformation of HeLa × Skin Fibroblast Human Cell Hybrids

1998 ◽  
Vol 149 (3) ◽  
pp. 246 ◽  
Author(s):  
Marc S. Mendonca ◽  
Kelly Howard ◽  
Clare L. Fasching ◽  
Daphne L. Farrington ◽  
Lael A. Desmond ◽  
...  
Keyword(s):  
Human Cell ◽  
Skin Fibroblast ◽  
Neoplastic Transformation ◽  
Cell Hybrids ◽  
Radiation Induced

A tumor-associated glycosylation change in the glucose transporter GLUT1 controlled by tumor suppressor function in human cell hybrids

1995 ◽  
Vol 108 (12) ◽  
pp. 3735-3743 ◽  
Author(s):  
T. Kitagawa ◽  
Y. Tsuruhara ◽  
M. Hayashi ◽  
T. Endo ◽  
E.J. Stanbridge
Keyword(s):  
Tumor Suppressor ◽  
Human Cell ◽  
Hela Cells ◽  
Glucose Transporter ◽  
Tumor Suppressor Function ◽  
Cell Hybrids ◽  
Putative Tumor Suppressor ◽  
Glycosylation Change ◽  
Glucose Transporter Glut1 ◽  
Transporter Glut1

Studies of human cell hybrids have provided evidence that the tumorigenicity of a cervical carcinoma (HeLa) is under the control of a putative tumor suppressor on chromosome 11. Using these human cell hybrids, we found a tumor-associated glycosylation change in the glucose transporter GLUT1, which is an N-linked glycoprotein at the plasma membrane. The non-tumorigenic HeLa × fibroblast cell hybrid CGL1 and the normal diploid fibroblast WI38 expressed the 50–55 kDa GLUT1, whereas in a tumorigenic segregant hybrid, CGL4, as well as in parental HeLa cells, GLUT1 glycosylation was altered and its molecular mass was about 70 kDa. However, the altered GLUT1 glycosylation was not observed in SV40-transformed WI38 cells, suggesting a correlation between this glycosylation change and a putative tumor suppressor function. Further investigations using glycosidases, glycosylation inhibitors and lectin-affinity chromatography demonstrated that the tumor-associated glycosylation change in GLUT1 was mainly due to the increase in N-acetyl-lactosamine repeats in the N-linked oligosaccharides. In accordance with the altered glycosylation, affinity for 2-deoxyglucose in the tumorigenic CGL4 cells increased 2-fold, but there was little change in the Vmax. These results suggest there may be a functional role for the modulation by glycosylation of GLUT1 in the tumorigenic behavior of CGL4 and HeLa cells.

Further Studies on the Radiation-Induced Expression of a Tumor-Specific Antigen in Human Cell Hybrids

1988 ◽  
Vol 114 (1) ◽  
pp. 84 ◽  
Author(s):  
C. Sun ◽  
J. L. Redpath ◽  
M. Colman ◽  
E. J. Stanbridge
Keyword(s):  
Human Cell ◽  
Specific Antigen ◽  
Induced Expression ◽  
Cell Hybrids ◽  
Radiation Induced ◽  
Tumor Specific Antigen

HIF1-α-Mediated Gene Expression Induced by Vitamin B1 Deficiency

2013 ◽  
Vol 83 (3) ◽  
pp. 188-197 ◽  
Author(s):  
Rebecca L. Sweet ◽  
Jason A. Zastre
Keyword(s):  
Gene Expression ◽  
Thiamine Deficiency ◽  
Glucose Transporter ◽  
Neuroblastoma Cell ◽  
Hypoxia Inducible Factor ◽  
Clinical Manifestations ◽  
Vitamin B1 ◽  
Low Oxygen ◽  
Glucose Transporter 1 ◽  
Metabolic Intermediates

It is well established that thiamine deficiency results in an excess of metabolic intermediates such as lactate and pyruvate, which is likely due to insufficient levels of cofactor for the function of thiamine-dependent enzymes. When in excess, both pyruvate and lactate can increase the stabilization of the hypoxia-inducible factor 1-alpha (HIF-1α) transcription factor, resulting in the trans-activation of HIF-1α regulated genes independent of low oxygen, termed pseudo-hypoxia. Therefore, the resulting dysfunction in cellular metabolism and accumulation of pyruvate and lactate during thiamine deficiency may facilitate a pseudo-hypoxic state. In order to investigate the possibility of a transcriptional relationship between hypoxia and thiamine deficiency, we measured alterations in metabolic intermediates, HIF-1α stabilization, and gene expression. We found an increase in intracellular pyruvate and extracellular lactate levels after thiamine deficiency exposure to the neuroblastoma cell line SK-N-BE. Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1α stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A. Both hypoxia and thiamine deficiency exposure resulted in an increase in the expression of the thiamine transporter SLC19A3. These results indicate thiamine deficiency induces HIF-1α-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency.

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