Abstract
The metabolic adaptations of cancer cells are receiving renewed attention as potential targets for therapeutic exploitation. Recent work has highlighted the importance of fatty acid catabolism through β-oxidation to cellular energy homeostasis. In this article, we describe recent preclinical studies suggesting that a gene usually expressed only in the brain, carnitine palmitoyltransferase (CPT)1C, promotes cancer cell survival and tumor growth. CTP1C confers rapamycin resistance on breast cancer cells, indicating that this gene may act in a pathway parallel to mTOR-enhanced glycolysis. Because of CPT1C's normally brain-restricted expression and the inability of most drugs to pass the blood-brain barrier, CPT1C may be an ideal candidate for specific small-molecule inhibition. We further speculate that concurrent targeting of CPT1C activity and glycolysis in tumor cells could be a highly effective anticancer approach.
Highlights
Cancer cell metabolism Tumor cells exhibit unique metabolic adaptations that are increasingly viewed as potential targets for novel and specific cancer therapies
Subsequent studies have shown that tumor cells exhibit several additional metabolic differences from normal cells, including an increased rate of glucose uptake that feeds a high rate of glycolysis, a more oxidative intracellular environment, and an ability to tolerate hypoxic conditions [3,4,5]
CPT1C as Anticancer Target metabolism in which parallel pathways involved in the regulation of fatty acid and glucose metabolism are proposed to provide ATP and antioxidants to cancer cells
Summary
Cancer cell metabolism Tumor cells exhibit unique metabolic adaptations that are increasingly viewed as potential targets for novel and specific cancer therapies. CPT1C as Anticancer Target metabolism in which parallel pathways involved in the regulation of fatty acid and glucose metabolism are proposed to provide ATP and antioxidants to cancer cells. Given the known activities of CPT1 proteins in catabolic energy generation in normal cells, it was theorized that CPT1C might be supplementing the high energy needs of cancer cells via FAO, and that cancers lacking CPT1C could not take advantage of this supplementation, and were sensitive to rapamycin.
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