Abstract
A high rate of aerobic glycolysis was catalyzed by rat-1 cells transfected with a ras oncogene (ras cells); rat-1 cells and rat-1 cells transfected with myc oncogene (myc cells) showed a low rate of glycolysis that was increased after exposure of the cells to type B transforming growth factor (TGF-beta). The uptake of radioactive methylaminoisobutyric acid or L-methionine via system A of amino acid transport also was accelerated after exposure of these cells to TGF-beta, with the myc cells being most sensitive and the ras cells least sensitive. Methionine was found to be a potent inhibitor of glycolysis in ras cells as well as in rat-1 or myc cells that were exposed to TGF-beta. We propose a relationship between the product of the ras oncogene (p21) and the protein(s) induced by exposure to TGF-beta.