Tumor suppressors and cell metabolism: a recipe for cancer growth.

By Russell G. Jones, Craig B. Thompson. Genes & Development, 2009

1,087 citations recorded by the source corpus.

Growing tumors face two major metabolic challenges-how to meet the bioenergetic and biosynthetic demands of increased cell proliferation, and how to survive environmental fluctuations in external nutrient and oxygen availability when tumor growth outpaces the delivery capabilities of the existing vasculature. Cancer cells display dramatically altered metabolic circuitry that appears to directly result from the oncogenic mutations selected during the tumorigenic process. An emerging theme in cancer biology is that many of the genes that can initiate tumorigenesis are intricately linked to metabolic regulation. In turn, it appears that a number of well-established tumor suppressors play critical roles in suppressing growth and/or proliferation when intracellular supplies of essential metabolites become reduced. In this review, we consider the potential role of tumor suppressors as metabolic regulators.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f40e1cdc46be710b4cc935547b39b521d22208fa

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Citations in the corpus

AMPK is a negative regulator of the Warburg Effect and suppresses tumor growth in vivo (2012, background): “Appreciation of the generality of the Warburg effect in cancer has stimulated the broader concept that a ‘‘metabolic transformation’’ accompanies tumorigenesis (Jones and Thompson, 2009).”
Hallmarks of cancer: the next generation. (2011, positive): “Similarly, TP53 null mice develop normally, show largely proper cell and tissue homeostasis, and again develop abnormalities later in life, in the form of leukemias and sarcomas (Ghebranious and Donehower, 1998).”
Targeting Free Radicals in Oxidative Stress-Related Human Diseases. (2017, background): “Because cancer cells are able to adapt to the altered redox homeostasis that results from their rapid growth, and can develop alternative metabolic pathways that make them less sensitive to exogenous stressors (which include chemotherapy and radiation [12]), an effective modulation of oxidative stre”
Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “…upstream regulating molecules and downstream metabolic products, known as metabolites, are altered (DeBerardinis et al., 2008b; Heiden et al., 2009; Jones and Thompson, 2009; Hanahan and Weinberg, 2011; DeBerardinis and Thompson, 2012; Hirschey et al., 2015; DeBerardinis and Chandel, 2016; Pavlova…”
Monoacylglycerol lipase regulates a fatty acid network that promotes cancer pathogenesis (2010, background): “The conversion of cells from a normal to cancerous state is accompanied by reprogramming of metabolic pathways (Deberardinis et al., 2008b; Jones and Thompson, 2009; Kroemer and Pouyssegur, 2008), including those that regulate glycolysis (Christofk et al., 2008; Gatenby and Gillies, 2004),…”
The lipid kinase PI5P4Kβ is an intracellular GTP sensor for metabolism and tumorigenesis (2016, neutral): “Mo their metabolism in order to cope with nutrient and energy stresses during tumorigenesis (Cantor and Sabatini, 2012; Jones and Thompson, 2009; Laderoute et al., 2006; Schafer et al., 2009).”
Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “Downstream of glycolysis, glucose-derived pyruvate can enter the TCA cycle and contribute to the production of mitochondrial citrate, which can then feed into de novo fatty acid synthesis upon its export to the cytoplasm (27).”
Metabolomics for Investigating Physiological and Pathophysiological Processes. (2019, background): “This work has suggested that many of these cancer genes play central roles in cellular metabolism and that their loss or mutation leads to a fundamental alteration of metabolism that leads to sustained tumor growth (213, 222, 342).”
Targeting cancer metabolism: a therapeutic window opens (2011, background): “Altered expression of metabolic enzymes or changes in the regulation of metabolic pathways also occurs downstream of many oncogenes and tumour suppressor genes, and cancers with specific genetic lesions are addicted to at least some of these metabolic change”
p53 and metabolism (2009, background): “The ability of p53 to suppress glycolysis and to promote oxidative phosphorylation might help to prevent the unrestrained glycolytic flux that is associated with malignant cell growth, and so represents another manifestation of the tumour-suppressive activity of p53 (Ref”
Functional genomics reveals serine synthesis is essential in PHGDH-amplified breast cancer (2011, neutral): “Cancer cells adapt their metabolic processes to drive macromolecular biosynthesis for rapid cell growth and proliferation (1,2).”