Regulation of cancer metabolism by oncogenes and tumor suppressors

• Published in: Methods in enzymology Vol. 542; p. 59
• Main Authors: Iurlaro, Raffaella, León-Annicchiarico, Clara Lucía, Muñoz-Pinedo, Cristina
• Format: Journal Article
• Language: English
• Published: United States 2014
• Subjects: Animals; Cell Hypoxia; Genes, myc; Genes, p53; Genes, Tumor Suppressor; Humans; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism; Neoplasms - genetics; Neoplasms - metabolism; Neoplasms - pathology; NF-kappa B - metabolism; Oncogenes; Phosphatidylinositol 3-Kinases - metabolism; Proto-Oncogene Proteins c-akt - metabolism; PTEN Phosphohydrolase - metabolism; ras Proteins - genetics; ras Proteins - metabolism; Retinoblastoma Protein - genetics; Retinoblastoma Protein - metabolism; Signal Transduction; mTOR; HIF-1; AKT; RAS; MYC; p53
• ISSN: 1557-7988
• DOI: 10.1016/B978-0-12-416618-9.00003-0

Cell proliferation requires the coordination of multiple signaling pathways as well as the provision of metabolic substrates. Nutrients are required to generate such building blocks and their form of utilization differs to significant extents between malignant tissues and their nontransformed counterparts. Thus, oncogenes and tumor suppressor genes regulate the proliferation of cancer cells also by controlling their metabolism. Here, we discuss the central anabolic functions of the signaling pathways emanating from mammalian target of rapamycin, MYC, and hypoxia-inducible factor-1. Moreover, we analyze how oncogenic proteins like phosphoinositide-3-kinase, AKT, and RAS, tumor suppressors such as phosphatase and tensin homolog, retinoblastoma, and p53, as well as other factors associated with the proliferation or survival of cancer cells, such as NF-κB, regulate cellular metabolism.