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Nutrient Deprivation Signals to p53 Vousden KH and Ryan KM. Nat Rev Cancer. 2009 Suppression of ChREBP Does not Activate AMPK Murphy, Biochemical Journal 2009 Overview of Mitochondrial ROS Production Increased ROS Level and Decreased Cellular Glutathione Level in ChREBP-deficient Cells Compared with Control Cells (HCT116 Cells) Antioxidant N-acetylcysteine (NAC) Reduces ChREBP Knockdown-induced p53 Activation (HCT116 Cells) Suppression of ChREBP Leads to a p53-dependent Reduction in Tumor Growth ChREBP is highly expressed in liver and colorectal cancer cells and critical for cancer cell proliferation Glucose Glucose Lactate Fatty acid Amino acid Nucleotide TCA cycle High ChREBP expression cancer cell proliferation Glucose Glucose Lactate Fatty acid Amino acid Nucleotide TCA cycle Low ChREBP expression cancer cell proliferation Nutrients (glucose, amino acid, fatty acid, lactate, etc.) ChREBP MondoA Mondo family Glycolysis, anabolic metabolism and proliferation in colorectal and liver cancer cells Our group studies transcriptional regulation in cancer cell metabolism Cancer cell lines Mouse models Clinical samples Lecture Objectives To provide a brief summary of the history of research in cancer metabolism To summarize the metabolic strategies in cancer cells To reveal genetic mechanisms behind the metabolic phenotypes in tumors To give an example of transcriptional regulation in cancer metabolism (our work on ChREBP) Part III To provide a brief summary of the history of research in cancer metabolism To summarize the metabolic strategies in cancer cells To reveal genetic mechanisms behind the metabolic phenotypes in tumors To give an example of transcriptional regulation in cancer metabolism (our work on ChREBP) Terms PI3K = Phosphatidylinositol 3-kinases Akt / PKB, a serine/threonine protein kinase P53, a transcription factor AMPK = AMP-activated protein kinase HIF = Hypoxia-inducible factor, a transcription fa