The biology of cancer: metabolic reprogramming fuels cell growth and proliferation.

By Ralph J. Deberardinis, J. Lum, G. Hatzivassiliou, Craig B. Thompson. Cell Metabolism, 2008

3,947 citations recorded by the source corpus.

Cell proliferation requires nutrients, energy, and biosynthetic activity to duplicate all macromolecular components during each passage through the cell cycle. It is therefore not surprising that metabolic activities in proliferating cells are fundamentally different from those in nonproliferating cells. This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types. We also consider regulation of these fluxes by cellular mediators of signal transduction and gene expression, including the phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR system, hypoxia-inducible factor 1 (HIF-1), and Myc, during physiologic cell proliferation and tumorigenesis.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2c13b73ce6123966a9f8c82b8f26d9e3fbc312b7

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Citations in the corpus

Role of PFKFB3-driven glycolysis in vessel sprouting. (2013, neutral): “First, despite a low intrinsic yield, the yield of ATP generation by glycolysis can exceed that by glucose oxidation, as long as glucose is not limiting (DeBerardinis et al., 2008; Vander Heiden et al., 2009).”
An Integrated Metabolic Atlas of Clear Cell Renal Cell Carcinoma (2016, neutral): “Dysregulated metabolism is a cancer hallmark and presents opportunities for cancer diagnostics, prognostics, and therapeutics (DeBerardinis et al., 2008; Hanahan and Weinberg, 2011; Hsu and Sabatini, 2008; Vander Heiden et al., 2009).”
Cutting Edge: Distinct Glycolytic and Lipid Oxidative Metabolic Programs Are Essential for Effector and Regulatory CD4+ T Cell Subsets (2011, background): “To meet these requirements, activated T cells decrease lipid oxidation and undergo a rapid increase in glycolysis (4).”
Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review). (2012, background): “In addition to mediating HIFs, mTOR directly upregulates the basic glycolytic processes, from glucose uptake to lactate formation (56,58,67).”
p53 regulates biosynthesis through direct inactivation of glucose-6-phosphate dehydrogenase (2011, background): “This metabolic signature (aerobic glycolysis or the Warburg effect) enables cancer cells to direct glucose to biosynthesis, supporting their rapid growth and proliferatio”
The GCN2‐ATF4 pathway is critical for tumour cell survival and proliferation in response to nutrient deprivation (2010, background): “Rapidly proliferating transformed cells have been shown to increase their nutrient uptake in excess of their bioenergetic needs and to divert metabolic programs towards pathways that support macromolecular biosynthesis to support their rapid growth (DeBerardinis et al, 2008).”
The Warburg effect: essential part of metabolic reprogramming and central contributor to cancer progression (2019, background): “This possibility was never anticipated by Warburg, his supporters and contemporaries (e.g. DeBerardinis et al. 2008; Vander Heiden et al. 2009; Cairns et al. 2011; Mihaylova and Shaw 2011; Ward and Thompson 2012; Amoedo et al. 2013; Soga 2013; Phan et al. 2014; Liberty and Locasale 2016; Bose and…”
Glutaminolysis activates Rag-mTORC1 signaling. (2012, background): “This addiction is partly explained by glutaminolysis as an anaplerotic requirement in sustaining the TCA cycle (DeBerardinis et al., 2008).”
Regulation of glycolysis by the hypoxia‐inducible factor (HIF): implications for cellular physiology (2020, background): “This increase in glycolytic metabolism promotes angiogenesis at the vascular forefront via endothelial tip cell PFKFB3, which when silenced, impairs vessel sprouting (De Bock et al. 2013).”
Glutaminolysis and Transferrin Regulate Ferroptosis (2015, background): “Through glutaminolysis, proliferating cells use L-Gln both as a nitrogen source for the biosynthesis of nucleotides, amino acids, and hexamine, and as an important carbon source for the tricarboxylic acid (TCA) cycle (DeBerardinis et al., 2008).”
Blinded by the Light: The Growing Complexity of p53. (2009, background): “Cell 137, May 1, 2009 ©2009 Elsevier Inc. 423 work with p53 to produce a specific cellular response (Figure 5).”
THE HISTONE DEACETYLASE SIRT6 IS A NOVEL TUMOR SUPPRESSOR THAT CONTROLS CANCER METABOLISM (2012, neutral): “However, growing evidence has demonstrated that metabolic reprogramming of cancer cells is a primary function of activated oncogenes and inactivated tumor suppressors (Dang, 2012; DeBerardinis et al., 2008; Ward and Thompson, 2012).”
Aerobic glycolysis: meeting the metabolic requirements of cell proliferation. (2011, neutral): “In proliferating cells, however, the TCA cycle serves as an important source of biosynthetic precursors (DeBerardinis et al 2008) in addition to providing ATP.”
Nrf2 redirects glucose and glutamine into anabolic pathways in metabolic reprogramming. (2012, background): “Metabolic activities in proliferating cells are fundamentally different from those in quiescent cells (DeBerardinis et al., 2008).”
The Warburg Effect: How Does it Benefit Cancer Cells? (2016, methodology): “In this scenario, the increased glucose consumption is used as a carbon source for anabolic processes needed to support cell proliferation [17, 26-32].”