The Control of the Metabolic Switch in Cancers by Oncogenes and Tumor Suppressor Genes

By Arnold J. Levine, Anna M. Puzio-Kuter. Science, 2010

1,233 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ef28114ce76a5d1b67fbcb9c06561e0c6ed2c81c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

In Molecular Biology

Citations in the corpus

AMPK is a negative regulator of the Warburg Effect and suppresses tumor growth in vivo (2012, background): “It is now appreciated that many of the predominant mutations observed in cancer also control tumor cell metabolism (Levine and Puzio-Kuter, 2010), suggesting that oncogene and tumor suppressor networks influence metabolism as part of their mode of action.”
ROS homeostasis and metabolism: a dangerous liason in cancer cells (2016, background): “essential precursors for building the macromolecules required to sustain growth and proliferation.(72,73) As a matter of fact, therapeutic modulation of glucose metabolism and transport has been widely utilized as an effective anticancer strategy.”
Lactate: a metabolic key player in cancer. (2011, background): “Glutaminolysis also enables synthesis of macromolecules in proliferating cells (4).”
The Warburg effect in tumor progression: Mitochondrial oxidative metabolism as an anti-metastasis mechanism (2014, background): “p53 has been shown to control glycolysis, oxidative phosphorylation, glutaminolysis, fatty acid oxidation, and redox [50] [78].”
Fatty acid uptake and lipid storage induced by HIF-1α contribute to cell growth and survival after hypoxia-reoxygenation. (2014, background): “Oncogenes upregulate the transcription of various glycolytic genes (Levine and Puzio-Kuter, 2010), and the tumor suppressor p53 has a role in regulating glycolysis and OXPHOS (Maddocks and Vousden, 2011; Vousden and Ryan, 2009).”
Aerobic glycolysis: meeting the metabolic requirements of cell proliferation. (2011, neutral): “…of stressed or damaged cells. p53 promotes mitochondrial respiration while inhibiting glycolysis by repressing glucose transporters, inhibiting the glycolytic enzyme phosphoglycerate mutase, and decreasing 27 the activity of PFK-1 through TIGAR (Cheung & Vousden 2010, Levine & Puzio-Kuter 2010).”
Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review). (2012, background): “In energy metabolism, HIF1 induces GLUT1 and GLUT3 expression and upregulates 9 of the 10 enzymes that function in glycolysis (52).”