Glucose transport in developing Ehrlich ascites tumor cells: parallel changes in the rate of glucose uptake and cytochalasin B binding activity during tumor development and methotrexate treatment.
The ability of Ehrlich ascites tumor cells to take up glucose increased progressively during the course of tumor development. Simultaneously as the rate of uptake rose, the density of a class of glucose-reversible binding sites for cytochalasin B on the cell surface also increased. In its stereospecificity requirement toward competing sugars and in its sensitivity to phloretin and diethylstilbestrol, this class of binding sites resembled the putative glucose carriers identified in various other cell systems and may represent the glucose transporter in Ehrlich ascites cells. Work with methotrexate (MTX) substantiated this view. Methotrexate arrested tumor growth, inhibited glucose uptake, and reduced the number of cytochalasin B binding sites. In both MTX-treated and untreated cells, the magnitude of changes in number of cytochalasin B binding sites closely paralleled and sufficiently accounted for the magnitude of changes in glucose uptake. Qualitative changes in the turnover and affinity for substrate of the putative glucose carrier need not be invoked.
D000818:Animals; D001667:Binding, Competitive; D001693:Biological Transport, Active; D001786:Blood Glucose / Q000032:analysis; D002286:Carcinoma, Ehrlich Tumor / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D002455:Cell Division / Q000187:drug effects; D003571:Cytochalasin B / Q000378:metabolism*; D003837:Deoxy Sugars / Q000378:metabolism*; D003847:Deoxyglucose / Q000378:metabolism*; D007700:Kinetics; D008727:Methotrexate / Q000627:therapeutic use*; D051379:Mice
D001786:Blood Glucose; D003837:Deoxy Sugars; D003571:Cytochalasin B; D003847:Deoxyglucose; D008727:Methotrexate