Abstract
Abstract Aerobic glycolysis is one of major metabolic changes found in cancer cells and is a valid target for cancer therapy. The nonmetabolizable glucose analogue, 2-deoxyglucose (2-DG) interferes with glucose metabolism and enhances chemotherapy/radiotherapy in cancer cells. We have investigated the mechanism of action by which 2-DG inhibits mammalian target of rapamycin (mTOR) activity. We found that 2-DG treatment led to decreased mTOR activity which was regulated by induction of Redd1 protein in both lung cancer cells and cervical cancer cells. We also found 2-DG treatment led to increased ATF4 protein expression and transcriptional activity. Suppression of ATF4 using siRNAs led to decrease of 2-DG induced Redd1 expression. Our data suggested that 2-DG induced Redd1 expression is regulated by the ATF4, leading to mTOR inhibition. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 297.
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