Author(s)

Ning Li, Wen Tan, Jing Li, Ping Li, Simon Lee, Yitao Wang, Yuewen Gong

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It is well known that malignant cells have accelerated glucose uptake and metabolism in order to maintain their fast proliferation rates. With the increased influx of glucose into cancer cells, glycolysis is facilitated through a coordinated regulation of metabolic enzymes and pyruvate consumption. Shiftting from mitochondrial oxidative phosphorylation to glycolysis and other pathways such as pentose phosphate pathway (PPP) and de novo fatty acid synthesis in the breast tumor provides not only energy but also the materials needed for cell proliferation. Glucose augmentation in tumor cells can be due to the elevated level of glucose transporter (GLUT) proteins, such as the over-expression of GLUT1 and expression of GLUT5 in breast cancers. Moreover, other factors such as hypoxia-inducible factor-1 (HIF-1), estrogen and growth factors are important modulators of glucose metabolism in the progression of breast carcinomas. Therapies targeting at the glycolytic pathway, fatty acid synthesis and GLUTs expression are currently being investigated. Restoring tumor cells to its normal glucose metabolic state would endow tumor specific and accessible treatment that targets glucose metabolism.

Breast Cancer, Glucose Transport, Glycolysis, Fatty Acid Synthesis, Mitochondrial Metabolism

N. Li, W. Tan, J. Li, P. Li, S. Lee, Y. Wang and Y. Gong, "Glucose Metabolism in Breast Cancer and its Implication in Cancer Therapy," International Journal of Clinical Medicine, Vol. 2 No. 2, 2011, pp. 110-128. doi: 10.4236/ijcm.2011.22022.