The Tumor Suppressor p53 Down-Regulates Glucose Transporters GLUT1 and GLUT4 Gene Expression

By Fabiana Schwartzenberg-Bar-Yoseph, M. Armoni, E. Karnieli. Cancer Research, 2004

735 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/3f62296509e5e7eca0bb5434192b87a1c5c3c2d9

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In Cancer Research

1. Robert James Gillies
2. David M. Sabatini
3. Robert A. Gatenby
4. Karen H. Vousden
5. W. Gu
6. K. Ryan
7. Carol Prives
8. I. Robey

In Molecular Biology

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2. Karen H. Vousden
3. Carol Prives
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In Oncology

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3. Yingming Zhao
4. David M. Sabatini
5. Carol Prives
6. N. Kon
7. K. Ryan
8. M. Guo

Citations in the corpus

• Causes and Consequences of Increased Glucose Metabolism of Cancers (2008, background): “Wild-type p53 can repress GLUT1 transcription, and mutations within the DNA-binding domain of p53, which are usually associated with malignancy, impair this repressive effect, thereby resulting in increased glucose metabolism and cell energy supply (148).”
• Phosphate-activated glutaminase (GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species (2010, background): “For example, p53 decreases the glycolytic rate through inhibiting expression of glucose transporters (6) and phosphoglycerate mutase (7) while increasing the expression of TIGAR that reduces fructose-2,6-bisphosphate levels (8).”
• p53 and metabolism (2009, background): “p53 can inhibit the expression of the glucose transporters GLUT1 and GLUT4 (Ref”
• Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “97 Glycolysis and gluconeo-genesis can be considered reversible processes to some extent. p53 inhibition of glycolysis promotes the process of gluconeogenesis.”
• Activation of SAT1 engages polyamine metabolism with p53-mediated ferroptotic responses (2016, neutral): “Proc Natl Acad Sci USA 107(16):7455–7460.”
• Tumor suppression in the absence of p53-mediated cell cycle arrest, apoptosis, and senescence (2012, positive): “For example p53 suppresses the expression of glucose transporters such as GLUT3 (Kawauchi et al., 2008; Schwartzenberg-Bar-Yoseph et al., 2004), although the precise mechanism of this repression needs further elucidation.”
• Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “For example, p53 transcriptionally induces both synthesis of cytochrome oxidase 2 (SCO2) (63) and TP53-induced glycolysis and apoptosis regulator (TIGAR) (64), while it represses expression of various glucose transporters (65), the glycolytic enzyme phosphoglycerate mutase (66), and PDK-2 (67) – a f”
• Reprogramming of glucose, fatty acid and amino acid metabolism for cancer progression (2015, background): “However, the tumor suppressor p53 decreases glucose uptake in cells by inhibiting transcription expression of GLUT1 and GLUT4 [16], or plays a key role in negative regulation of glycolysis under normoxic conditions or hypoxic conditions through its targets [17].”