The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
p53 regulates biosynthesis through direct inactivation of glucose-6-phosphate dehydrogenase
Open accessAbstract
Cancer cells consume large quantities of glucose and primarily use glycolysis for ATP production, even in the presence of adequate oxygen. This metabolic signature (aerobic glycolysis or the Warburg effect) enables cancer cells to direct glucose to biosynthesis, supporting their rapid growth and proliferation. However, both causes of the Warburg effect and its connection to biosynthesis are not well understood. Here we show that the tumour suppressor p53, the most frequently mutated gene in human tumours, inhibits the pentose phosphate pathway (PPP). Through the PPP, p53 suppresses glucose consumption, NADPH production and biosynthesis. The p53 protein binds to glucose-6-phosphate dehydrogenase (G6PD), the first and rate-limiting enzyme of the PPP, and prevents the formation of the active dimer. Tumour-associated p53 mutants lack the G6PD-inhibitory activity. Therefore, enhanced PPP glucose flux due to p53 inactivation may increase glucose consumption and direct glucose towards biosynthesis in tumour cells.
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“p53 binds to G6PDH, the rate-limiting enzyme of the pentose phosphate pathway, to further inhibit the activated pentose phosphate pathway in tumor cells.95,96”
From Targeting p53 pathways: mechanisms, structures, and advances in therapy (2023) · cites this paper as [95]
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Cites
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“The tumour suppressor p53 invokes anti-proliferative processes, of which the best understood include cell cycle arrest, DNA repair and apoptosi”
BackgroundThe Biology of Cancer: Metabolic Reprogramming Fuels Cell Growth and Proliferation
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p53 Regulates Mitochondrial Respiration
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A Chemical Inhibitor of p53 That Protects Mice from the Side Effects of Cancer Therapy
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Glycolytic Enzymes Can Modulate Cellular Life Span
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The emerging hallmarks of cancer metabolism
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The PI3K–AKT network at the interface of oncogenic signalling and cancer metabolism
Hoxhaj, G., & Manning, B. D. (2020) · Nature Reviews Cancer · doi:10.1038/s41568-019-0216-7 · Cited by 2,137
Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism
Ying, H., Kimmelman, A. C., Lyssiotis, C. A., Hua, S., Chu, G. C., Fletcher-Sananikone, E., Locasale, J. W., Son, J., Zhang, H., Coloff, J. L., et al. (2012) · Cell · doi:10.1016/j.cell.2012.01.058 · Cited by 2,043
The return of metabolism: biochemistry and physiology of the pentose phosphate pathway
Stincone, A., Prigione, A., Cramer, T., Wamelink, M. M. C., Campbell, K., Cheung, E., Olin‐Sandoval, V., Grüning, N., Krüger, A., Tauqeer Alam, M., et al. (2015) · Biological Reviews · doi:10.1111/brv.12140 · Cited by 1,576
The pentose phosphate pathway and cancer
Patra, K. C., & Hay, N. (2014) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2014.06.005 · Cited by 1,432
Metadata
- Authors
- Jiang, P., Du, W., Wang, X., Mancuso, A., Gao, X., Wu, M., & Yang, X.
- Venue
- Nature Cell Biology
- Published
- 2011-02-20
- Volume
- 13
- Issue
- 3
- Pages
- 310-316
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W2046100445
- Cited by
- 795
- References
- 10
- FWCI
- 15.51
- Type
- journal article
- Language
- en
- Open access
- green
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