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Genetic alterations that involve mutations in oncogenes and/or tumor suppressor genes lead to deregulated signaling pathways and consequently to the aberrant expression of transcription factors, enzymes, transporters, proteins (nuclear and cytoplasmic), and regulatory molecules of glucose metabolism ( FIGURE 1 The phosphoinositide 3-kinase-Akt-mammalian target of rapamycin (PI3K-Akt-mTOR) signaling pathway, commonly activated in cancer, including AML, contributes to the maintenance of glycolysis by translational and post-translational regulation of metabolic enzymes ( A master transcription factor in the regulation of glycolysis is hypoxia-inducible factor 1 (HIF-1) because it promotes the transcription of glucose transporters, such as glucose transporter 1 (GLUT1), and glycolytic enzymes, such as hexokinase II (HK-II), and pyruvate kinase M2 (PKM2) ( Another molecule that promotes glycolysis is the proliferating cell nuclear antigen (PCNA), which is a nuclear protein synthesized in the early G1 phase and in the S phase of the cell cycle and is considered a marker of the proliferation index in some neoplasms ( On the other hand, the enzyme heme oxygenase-1 (HO-1) catalyzes the degradation of the heme group, causing carbon monoxide (CO), biliverdin, and iron, where the heme group is a critical component of multiple hemoproteins involved in glucose metabolism and of lipids and proteins

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XIAP-ULK1-mediated mitophagy modulates carnitine metabolism to mitigate diabetic kidney disease