ArticleProceedings of the National Academy of Sciences of the United States of America1999
An inducible gene product for 6-phosphofructo-2-kinase with an AU-rich instability element: role in tumor cell glycolysis and the Warburg effect.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 287 citations in OpenAlex.
- F26BP enables control of glycolysis rate independent of energy state.bioRxiv : the preprint server for biology · 2026Article
- PFKFB3 Mediated Glycolytic Reprogramming Drives Vascular Endothelial Injury Under Chronic Intermittent Hypoxia.International journal of biological sciences · 2026Article
- PFKFB3-Inhibitor 3PO-Mediated Glycolytic Reprogramming Promotes Inflammatory Dental Pulp Repair: An In Vitro and In Vivo Study.International endodontic journal · 2025Article
- Review
- Plasma metabolomic signatures for copy number variants and COVID-19 risk loci in Northern Finland populations.Scientific reports · 2025Article
- PFKFB3 Connects Glycolytic Metabolism with Endothelial Dysfunction in Human and Rodent Obesity.Antioxidants (Basel, Switzerland) · 2025Article
- Repression of PFKFB3 sensitizes ovarian cancer to PARP inhibitors by impairing homologous recombination repair.Cell communication and signaling : CCS · 2025Article
- rTM reprograms macrophages via the HIF-1α/METTL3/PFKM axis to protect mice against sepsis.Cellular and molecular life sciences : CMLS · 2024Article
- Role of PFKFB3-driven glycolysis in sepsis.Annals of medicine · 2023Review
- Trigred motif 36 regulates neuroendocrine differentiation of prostate cancer via HK2 ubiquitination and GPx4 deficiency.Cancer science · 2023Article
- Targeting Aurora-A inhibits tumor progression and sensitizes thyroid carcinoma to Sorafenib by decreasing PFKFB3-mediated glycolysis.Cell death & disease · 2023Article
- Hyperglycemia induces PFKFB3 overexpression and promotes malignant phenotype of breast cancer through RAS/MAPK activation.World journal of surgical oncology · 2023Article
- Review
- Synthesis, radiolabeling, and evaluation of 68Ga-labeled aminoquinoxaline derivative as a potent PFKFB3-targeted PET tracer.Frontiers in chemistry · 2023Article
- Mutation of regulatory phosphorylation sites in PFKFB2 does not affect the anti-fibrotic effect of metformin in the kidney.PloS one · 2023Article
- HIF1A-dependent induction of alveolar epithelial PFKFB3 dampens acute lung injury.JCI insight · 2022Article
- KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells.Communications biology · 2022Article
- Multiomics analysis couples mRNA turnover and translational control of glutamine metabolism to the differentiation of the activated CD4Scientific reports · 2022Article
- The role of PFKFB3 in maintaining colorectal cancer cell proliferation and stemness.Molecular biology reports · 2022Review
- A miR-34a-guided, tRNACell death discovery · 2022Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells maintain a high glycolytic rate even in the presence of oxygen, a phenomenon first described over 70 years ago and known historically as the Warburg effect. Fructose 2,6-bisphosphate is a powerful allosteric regulator of glycolysis that acts to stimulate the activity of 6-phosphofructo-1-kinase (PFK-1), the most important control point in mammalian glycolysis. The steady state concentration of fructose 2,6-bisphosphate in turn depends on the activity of the enzyme 6-phosphofructo-2-kinase (PFK-2)/fructose-2, 6-bisphosphatase, which is expressed in several tissue-specific isoforms. We report herein the identification of a gene product for this enzyme that is induced by proinflammatory stimuli and which is distinguished by the presence of multiple copies of the AUUUA mRNA instability motif in its 3'-untranslated end. This inducible gene for PFK-2 is expressed constitutively in several human cancer cell lines and was found to be required for tumor cell growth in vitro and in vivo. Inhibition of inducible PFK-2 protein expression decreased the intracellular level of 5-phosphoribosyl-1-pyrophosphate, a product of the pentose phosphate pathway and an important precursor for nucleic acid biosynthesis. These studies identify a regulatory isoenzyme that may be essential for tumor growth and provide an explanation for long-standing observations concerning the apparent coupling of enhanced glycolysis and cell proliferation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.