ArticleMolecular and cellular biochemistry2020
PFKFB2 regulates glycolysis and proliferation in pancreatic cancer cells.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- Orchestrating glucose metabolism: PFKFB2 as a signal-integrating conductor in homeostasis and disease.The Journal of biological chemistry · 2026Review
- Carbohydrates metabolic reprogramming and tumor microenvironment in pancreatic cancer: targeting pathways.Molecular biology reports · 2026Review
- High-Glucose-Induced Metabolic and Epithelial Stress in Grass Carp Intestinal Epithelial Cells Associated with Methylation-Related Transcriptional Responses.International journal of molecular sciences · 2026Article
- Glycolytic reprogramming in endometriosis: molecular mechanisms, immune modulation, and non-hormonal therapeutic opportunities.BMC women's health · 2026Review
- THAP7-AS1 sponges miR-4286 to upregulate PFKFB2, accelerating aerobic glycolysis and aggravating liver cancer progression.Frontiers in cell and developmental biology · 2026Article
- Brain-specific expression of cytomegalovirus immediate early protein 1 disrupts neurodevelopment in mice by inducing neuroinflammation and altering astrocytic metabolism.Virology journal · 2025Article
- Transcriptome Sequencing Reveals Effects of Artificial Feed Domestication on Intestinal Performance and Gene Expression of Carnivorous Mandarin Fish (Siniperca chuatsi) and Related Mechanisms.Marine biotechnology (New York, N.Y.) · 2025Article
- Emerging Trends in Gastrointestinal Cancer Targeted Therapies: Harnessing Tumor Microenvironment, Immune Factors, and Metabolomics Insights.Gastroenterology · 2024Review
- Emerging roles of lactate in acute and chronic inflammation.Cell communication and signaling : CCS · 2024Review
- HP promotes neutrophil inflammatory activation by regulating PFKFB2 in the glycolytic metabolism of sepsis.PloS one · 2024Article
- Hitting the Sweet Spot: How Glucose Metabolism Is Orchestrated in Space and Time by Phosphofructokinase-1.Cancers · 2023Review
- Loss of function of ribosomal protein L13a blocks blastocyst formation and reveals a potential nuclear role in gene expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- miR-21-5p inhibits the growth of brain glioma cells through regulating the glycolysis mediated by PFKFB2.Functional & integrative genomics · 2023Article
- Formyl-peptide receptor 2 signalling triggers aerobic metabolism of glucose through Nox2-dependent modulation of pyruvate dehydrogenase activity.Open biology · 2023Article
- Expression of Pfkfb isoenzymes during in vitro differentiation of mouse embryonic stem cells into insulin-producing cells.Turkish journal of medical sciences · 2023Article
- Long non-coding RNAs involved in retinoblastoma.Journal of cancer research and clinical oncology · 2023Review
- Knockdown circZNF131 Inhibits Cell Progression and Glycolysis in Gastric Cancer Through miR-186-5p/PFKFB2 Axis.Biochemical genetics · 2022Article
- A transcriptomic signature for prostate cancer relapse prediction identified from the differentially expressed genes between TP53 mutant and wild-type tumors.Scientific reports · 2022Article
- Exosomal circCARM1 from spheroids reprograms cell metabolism by regulating PFKFB2 in breast cancer.Oncogene · 2022Article
- Article
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Tumor cells increase glucose metabolism through glycolysis and pentose phosphate pathways to meet the bioenergetic and biosynthetic demands of rapid cell proliferation. The family of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFB1-4) are key regulators of glucose metabolism via their synthesis of fructose-2,6-bisphosphate (F2,6BP), a potent activator of glycolysis. Previous studies have reported the co-expression of PFKFB isozymes, as well as the mRNA splice variants of particular PFKFB isozymes, suggesting non-redundant functions. Majority of the evidence demonstrating a requirement for PFKFB activity in increased glycolysis and oncogenic properties in tumor cells comes from studies on PFKFB3 and PFKFB4 isozymes. In this study, we show that the PFKFB2 isozyme is expressed in tumor cell lines of various origin, overexpressed and localizes to the nucleus in pancreatic adenocarcinoma, relative to normal pancreatic tissue. We then demonstrate the differential intracellular localization of two PFKFB2 mRNA splice variants and that, when ectopically expressed, cytoplasmically localized mRNA splice variant causes a greater increase in F2,6BP which coincides with an increased glucose uptake, as compared with the mRNA splice variant localizing to the nucleus. We then show that PFKFB2 expression is required for steady-state F2,6BP levels, glycolytic activity, and proliferation of pancreatic adenocarcinoma cells. In conclusion, this study may provide a rationale for detailed investigation of PFKFB2's requirement for the glycolytic and oncogenic phenotype of pancreatic adenocarcinoma cells.
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Registered trials
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.