Fructose-2,6-Bisphosphate synthesis by 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase 4 (PFKFB4) is required for the glycolytic response to hypoxia and tumor growth
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Summary
It is found that PFKFB4 is required for cancer cell survival during the metabolic response to hypoxia, presumably to enable glycolytic production of ATP when the electron transport chain is not fully operational.
- Type
- article
- Published
- 2014-07-13
- Cited by
- 83
- References
- 33
- Access
- Open access
- OpenAlex
- https://openalex.org/W1511847298
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:6082655
Keywords
Phosphofructokinase 2, Fructose 2,6-bisphosphate, Glycolysis, Anaerobic glycolysis, Medicine
References
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- Hypoxic regulation of the 6‐phosphofructo‐2‐kinase/fructose‐2,6‐bisphosphatase gene family (PFKFB‐1–4) expression in vivo
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- Ras transformation requires metabolic control by 6-phosphofructo-2-kinase
- A kinetic study of pyrophosphate: fructose-6-phosphate phosphotransferase from potato tubers. Application to a microassay of fructose 2,6-bisphosphate.
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- Estradiol Stimulates Glucose Metabolism via 6-Phosphofructo-2-kinase (PFKFB3)*
- Hypoxia induces transcription of 6‐phosphofructo‐2‐kinase/fructose‐2,6‐biphosphatase‐4 gene via hypoxia‐inducible factor‐1α activation
- Overexpression of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-4 in the human breast and colon malignant tumors.
- Increased Concentrations of Fructose 2,6-Bisphosphate Contribute to the Warburg Effect in Phosphatase and Tensin Homolog (PTEN)-deficient Cells*
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- The human ubiquitous 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase gene (PFKFB3): promoter characterization and genomic structure.
Cited by
- Organ-Specific Cancer Metabolism and Its Potential for Therapy.
- Enzyme kinetics : 6-phosphofructo-2-kinase/2,6-bisphosphatase.
- Proteomic and functional profiles of a follicle‐stimulating hormone positive human nonfunctional pituitary adenoma
- Targeting the sugar metabolism of tumors with a first-in-class 6-phosphofructo-2-kinase (PFKFB4) inhibitor
- Enhancement of angiogenic effects by hypoxia‐preconditioned human umbilical cord‐derived mesenchymal stem cells in a mouse model of hindlimb ischemia
- INHIBITION OF IRE1 MODIFIES EFFECT OF GLUCOSE DEPRIVATION ON THE EXPRESSION OF TNFα-RELATED GENES IN U87 GLIOMA CELLS.
- Hypoxic regulation of the expression of cell proliferation related genes in U87 glioma cells upon inhibition of ire1 signaling enzyme
- HIF-1α activates hypoxia-induced PFKFB4 expression in human bladder cancer cells.
- Inhibition of IRE1 signaling affects expression of a subset genes encoding for TNF-related factors and receptors and modifies their hypoxic regulation in U87 glioma cells
- In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity
- Metabonomics applied in exploring the antitumour mechanism of physapubenolide on hepatocellular carcinoma cells by targeting glycolysis through the Akt-p53 pathway
- IRE-1α regulates expression of ubiquitin specific peptidases during hypoxic response in U87 glioma cells
- Inhibition of 6-phosphofructo-2-kinase (PFKFB3) suppresses glucose metabolism and the growth of HER2+ breast cancer
- Genome-wide landscape of DNA methylomes and their relationship with mRNA and miRNA transcriptomes in oxidative and glycolytic skeletal muscles
- Phosphorylation of PPARγ at Ser84 promotes glycolysis and cell proliferation in hepatocellular carcinoma by targeting PFKFB4
- Hypoxic regulation of MYBL1, MEST, TCF3, TCF8, GTF2B, GTF2F2 and SNAI2 genes expression in U87 glioma cells upon IRE1 inhibition.
- 6-Phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 is essential for p53-null cancer cells
- 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase-3 is required for transforming growth factor β1-enhanced invasion of Panc1 cells in vitro.
- Loss of PFKFB4 induces cell death in mitotically arrested ovarian cancer cells
- Expression of ubiquitin specific peptidase genes in IRE1 knockdown U87 glioma cells upon glucose deprivation
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