TIGAR Protein Promotes Growth of Breast Cancer by Altering Cell Metabolism That Can Be Targeted with Existing Drugs

How does a cancer cell burn calories? New research from Thomas Jefferson University in Philadelphia shows that breast cancer cells rely on a different process for turning fuel into energy than normal cells. The results were published online on November 1, 2016 in the Journal of Biological Chemistry. The JBC article is titled “TIGAR Metabolically Reprograms Carcinoma and Stromal Cells in Breast Cancer." “Our finding is part of a growing interest in studying the metabolic function of cancer," says Ubaldo Martinez-Outschoorn, M.D., Assistant Professor in the Department of Medical Oncology at Thomas Jefferson University and researcher at the Sidney Kimmel Cancer Center at Jefferson. "The better we understand how cancers thrive, the better we'll be able to cut off the energy supply they need for survival." Dr. Martinez-Outschoorn and colleagues looked at a protein that they knew changed the metabolism of breast cancer cells. The protein TIGAR (short for TP53 inducible glycolysis and apoptosis regulator) diminished the cell's ability to create energy via the most common biochemical pathway -- converting sugar to energy via glycolysis. But it was unclear how this change in metabolism altered the cancer cell, or how the cell was getting the energy it needed to survive. Through a series of cellular and mouse studies, the researchers demonstrated that breast cancer cells with a higher-than-normal abundance of the TIGAR protein were more aggressive and were able to grow faster than breast cancer cells that had normal amounts of TIGAR. But if the cells weren't using glycolysis to drive this growth, what were they using? Dr. Martinez-Outschoorn and colleagues showed that when cells expressed TIGAR, they swap their metabolic pathway and become dependent on mitochondria for energy production.
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