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  Indian J Med Microbiol
 

Figure 2: Overview of metabolism of normal cells and the reprogrammed metabolism of cancer cells. Under normal condition, cells mainly depend on OXPHOS for the generation of ATP. Without the presence of external stimulus, the PI3K-AKT pathway remains inactive and the low level activity of AMPK keeps the action of mTOR and HIF1α in check. Cancer cells reprogram their metabolism in a way that they mainly depend on glucose and glycolysis for ATP generation. Oncogenic signals act as the stimuli to promote PI3K-AKT pathway and suppress AMPK activity and thus induce the expression of glycolytic genes. Hypoxia also induces the expression of HIF1α and thus increases the expression of glucose transporters and other glycolytic genes. Besides this the expression of IDO induces catabolism of tryptophan and that in a way increase the nucleotide, amino acid, and lipid biosynthesis and thus help in the rapid proliferation of cancer cells. Akt1: Protein kinase B, AMPK: AMP-activated protein kinase, ASCT2: alanine, serine, and cysteine system amino acids transporter-2, ATP: Adenosine triphosphate, Glut1/4: Glucose transporter1/4, HIF1α: Hypoxia-inducible factor-1α, HK: Hexokinase, IDO: Indoleamine-pyrrole 2,3-dioxygenase, Mtor: Mechanistic/mammalian target of rapamycin, PI3K: Phosphatidylinositol-4,5-bisphosphate 3-kinase, OXPHOS: Oxidative phosphorylation

Figure 2: Overview of metabolism of normal cells and the reprogrammed metabolism of cancer cells. Under normal condition, cells mainly depend on OXPHOS for the generation of ATP. Without the presence of external stimulus, the PI3K-AKT pathway remains inactive and the low level activity of AMPK keeps the action of mTOR and HIF1α in check. Cancer cells reprogram their metabolism in a way that they mainly depend on glucose and glycolysis for ATP generation. Oncogenic signals act as the stimuli to promote PI3K-AKT pathway and suppress AMPK activity and thus induce the expression of glycolytic genes. Hypoxia also induces the expression of HIF1α and thus increases the expression of glucose transporters and other glycolytic genes. Besides this the expression of IDO induces catabolism of tryptophan and that in a way increase the nucleotide, amino acid, and lipid biosynthesis and thus help in the rapid proliferation of cancer cells. Akt1: Protein kinase B, AMPK: AMP-activated protein kinase, ASCT2: alanine, serine, and cysteine system amino acids transporter-2, ATP: Adenosine triphosphate, Glut1/4: Glucose transporter1/4, HIF1α: Hypoxia-inducible factor-1α, HK: Hexokinase, IDO: Indoleamine-pyrrole 2,3-dioxygenase, Mtor: Mechanistic/mammalian target of rapamycin, PI3K: Phosphatidylinositol-4,5-bisphosphate 3-kinase, OXPHOS: Oxidative phosphorylation