Links between metabolism and cancer.

By C. V. Dang. Genes & Development, 2012

1,006 citations recorded by the source corpus.

Metabolism generates oxygen radicals, which contribute to oncogenic mutations. Activated oncogenes and loss of tumor suppressors in turn alter metabolism and induce aerobic glycolysis. Aerobic glycolysis or the Warburg effect links the high rate of glucose fermentation to cancer. Together with glutamine, glucose via glycolysis provides the carbon skeletons, NADPH, and ATP to build new cancer cells, which persist in hypoxia that in turn rewires metabolic pathways for cell growth and survival. Excessive caloric intake is associated with an increased risk for cancers, while caloric restriction is protective, perhaps through clearance of mitochondria or mitophagy, thereby reducing oxidative stress. Hence, the links between metabolism and cancer are multifaceted, spanning from the low incidence of cancer in large mammals with low specific metabolic rates to altered cancer cell metabolism resulting from mutated enzymes or cancer genes.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/328405abef56d7bab30156077b6df6e78a026550

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Citations in the corpus

KRAS: feeding pancreatic cancer proliferation (2014, neutral): “Glutamine contributes to macromolecular synthesis in cancer cells by providing carbon to fuel the TCA cycle and nitrogen for nucleotide, nonessential amino acid (NEAA), and hexosamine biosynthesis [43,44].”
Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging (2013, background): “This metabolic reprogramming, known as the Warburg effect (Warburg, 1956), is driven by several different pathways, includingmTOR, c-Myc, and hypoxia-inducible factor 1 (HIF-1a) (Dang, 2012).”
Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “Though glucose catabolism through aerobic glycolysis has in large part become synonymous with the hallmark designation attributed to altered cancer metabolism, it alone cannot explain all the metabolic changes that may be necessary to support the requirements of cell growth (17).”
ROS homeostasis and metabolism: a dangerous liason in cancer cells (2016, background): “Otto Warburg in the 1924, tumor cells exhibit a prevalent use of the glycolytic pathway regardless the presence of sufficient oxygen tension, a phenomenon known as Warburg effect.(64)”
Tumor glycolysis as a target for cancer therapy: progress and prospects (2013, background): “tumor glycolysis will impact tumor growth by energy depletion as well as sensitization to therapeutics especially, in light of the recent reports that have elucidated cancer-specific advantages of aerobic glycolysis [10-13].”
Fundamentals of cancer metabolism (2016, background): “Today, it is clear that cancer cells exhibit aerobic glycolysis due to activation of oncogenes, loss of tumor suppressors, and up-regulation of the PI3K pathway, and that one advantage of high glycolytic rates is the availability of precursors for anabolic pathways (2, 61).”
Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF (2013, neutral): “Similarly, the dysregulation of the proto-oncogene MYC leads to profound effects on tumor metabolism through multiple mechanisms (reviewed in Dang, 2012).”
Glutamine and cancer: cell biology, physiology, and clinical opportunities. (2013, positive): “Interest in cancer metabolism was boosted by discoveries that oncogenes and tumor suppressors could regulate nutrient metabolism, and that mutations in some metabolic enzymes participate in the development of malignancy (2, 3).”
Reprogramming of glucose, fatty acid and amino acid metabolism for cancer progression (2015, background): “Alterations of oncogenes and tumor suppressors drive cancer cells to aerobic glycolysis through regulation of metabolic enzymes [30].”
Lactate in the Regulation of Tumor Microenvironment and Therapeutic Approaches (2019, background): “It has been shown that metabolic alterations play an important role in cancer development, progression and maintenance (131).”
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].”