title: Oncogenic regulation of tumor metabolic reprogramming.
abstract: Development of malignancy is accompanied by a complete metabolic reprogramming closely related to the acquisition of most of cancer hallmarks. In fact, key oncogenic pathways converge to adapt the metabolism of carbohydrates, proteins, lipids and nucleic acids to the dynamic tumor microenvironment, conferring a selective advantage to cancer cells. Therefore, metabolic properties of tumor cells are significantly different from those of non-transformed cells. In addition, tumor metabolic reprogramming is linked to drug resistance in cancer treatment. Accordingly, metabolic adaptations are specific vulnerabilities that can be used in different therapeutic approaches for cancer therapy. In this review, we discuss the dysregulation of the main metabolic pathways that enable cell transformation and its association with oncogenic signaling pathways, focusing on the effects of c-MYC, hypoxia inducible factor 1 (HIF1), phosphoinositide-3-kinase (PI3K), and the mechanistic target of rapamycin (mTOR) on cancer cell metabolism. Elucidating these connections is of crucial importance to identify new targets and develop selective cancer treatments that improve response to therapy and overcome the emerging resistance to chemotherapeutics.
authors.affiliation: Department of Biochemistry and Molecular Biomedicine, Universitat de Barcelona, Institute of Biomedicine of Universitat de Barcelona (IBUB) and CSIC-Associated Unit, Barcelona, Spain.
authors.forename: Míriam
authors.initials: M
authors.lastname: Tarrado-Castellarnau
authors.affiliation: Department of Biochemistry and Molecular Biomedicine, Universitat de Barcelona, Institute of Biomedicine of Universitat de Barcelona (IBUB) and CSIC-Associated Unit, Barcelona, Spain.
authors.forename: Pedro
authors.initials: P
authors.lastname: de Atauri
authors.affiliation: Department of Biochemistry and Molecular Biomedicine, Universitat de Barcelona, Institute of Biomedicine of Universitat de Barcelona (IBUB) and CSIC-Associated Unit, Barcelona, Spain.
authors.forename: Marta
authors.initials: M
authors.lastname: Cascante
mesh_terms: D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D014408:Biomarkers, Tumor / Q000378:metabolism; D063646:Carcinogenesis; D002453:Cell Cycle; D002471:Cell Transformation, Neoplastic; D015972:Gene Expression Regulation, Neoplastic; D006019:Glycolysis; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D050356:Lipid Metabolism; D008055:Lipids / Q000737:chemistry; D008928:Mitochondria / Q000378:metabolism; D009369:Neoplasms / Q000378:metabolism; D009857:Oncogenes; D018384:Oxidative Stress; D010100:Oxygen / Q000737:chemistry; D010427:Pentose Phosphate Pathway; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D059016:Tumor Microenvironment
chemical_list: D000596:Amino Acids; D014408:Biomarkers, Tumor; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D008055:Lipids; D010100:Oxygen; D019869:Phosphatidylinositol 3-Kinases; D016271:Proto-Oncogene Proteins c-myc; D058570:TOR Serine-Threonine Kinases; C497442:HIF1A protein, human; C546842:MTOR protein, human
keywords: HIF; MYC; PI3K; mTOR; metabolic reprogramming