These phase contrast and confocal immunofluorescence images (inset)show 3D cultures of non-malignant (S1) and malignant (T4-2) human breast cells in which glucose metabolism is inhibited by the addition of 2-deoxy-D-glucose (2DG). Suppressing glucose uptake leads to a phenotypic reversion of malignant cells (they look normal) while not affecting the non-malignant cells. (Click to enlarge)
Metabolism was lost in the shadows of cancer research for decades but has recently been reclaiming some of the spotlight. Now, Mina Bissell, Distinguished Scientist with Berkeley Lab's Life Sciences Division and a leading authority on breast cancer, has shown that aerobic glycolysis - glucose metabolism in the presence of oxygen - is not the consequence of the cancerous activity of malignant cells but is itself a cancerous event. "A dramatic increase in sugar uptake could be a cause of oncogenesis," Bissell says. "Furthermore, through a series of painstaking analysis, we have discovered two new pathways through which increased uptake of glucose could itself activate other oncogenic pathways. This discovery provides possible new targets for diagnosis and therapeutics." Working with Bissell, Yasuhito Onodera, a Japanese postdoctoral fellow in her research group who is now an assistant professor in Japan, examined the expression of glucose transporter proteins in human breast cells. The focus was on the glucose transporter known as GLUT3, the concentrations of which Onodera and Bissell showed are 400 times greater in malignant than in non-malignant breast cells. The study was carried out using a 3D culture assay developed earlier by Bissell and her group for mouse mammary cells and later with her collaborator, Ole Petersen, for human breast cells.
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