ArticleOncotarget2016
The platelet isoform of phosphofructokinase contributes to metabolic reprogramming and maintains cell proliferation in clear cell renal cell carcinoma.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Network-based gene deletion analysis identifies candidate genes and molecular mechanism involved in clear cell renal cell carcinoma.Journal of genetics · 2021Pooled it
- CSCN: inference of cell-specific causal networks using single-cell RNA-seq data.Bioinformatics (Oxford, England) · 2026Article
- PFKP in malignant tumors: bridging metabolic reprogramming, post-translational modifications, and the immunosuppressive microenvironment.Frontiers in cell and developmental biology · 2026Review
- Prediction of high-quality human oocytes and embryos through the analysis of gene expression in cumulus cells.Journal of ovarian research · 2025Review
- Catabolic rewiring in cancer impacts dietary interventions.Communications biology · 2025Review
- Phosphofructokinase-1 redefined: a metabolic hub orchestrating cancer hallmarks through multi-dimensional control networks.Journal of translational medicine · 2025Review
- Mitoquinol improves phagocytosis and glycolysis in ethanol-exposed macrophages via HIF-1α-PFKP axis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Emerging roles of metabolic biomarkers in renal cell carcinoma: from molecular mechanisms to clinical implications.Frontiers in cell and developmental biology · 2025Review
- Metabolic reprogramming and renal fibrosis: what role might Chinese medicine play?Chinese medicine · 2024Review
- Quercetin Impairs the Growth of Uveal Melanoma Cells by Interfering with Glucose Uptake and Metabolism.International journal of molecular sciences · 2024Article
- Metabolic alterations in hereditary and sporadic renal cell carcinoma.Nature reviews. Nephrology · 2024Review
- Glycolysis regulator PFKP induces human melanoma cell proliferation and tumor growth.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Bioinformatics identification of prognostic genes and potential interaction analysis in renal cell carcinoma.Translational cancer research · 2023Article
- RNAi screening reveals a synthetic chemical-genetic interaction between ATP synthase and PFK1 in cancer cells.Cancer science · 2023Article
- PFKP: More than phosphofructokinase.Advances in cancer research · 2023Review
- Phosphofructokinase Platelet Overexpression Accelerated Colorectal Cancer Cell Growth and Motility.Journal of Cancer · 2023Article
- NAD+ depletion enhances reovirus-induced oncolysis in multiple myeloma.Molecular therapy oncolytics · 2022Article
- SIRT2-PFKP interaction dysregulates phagocytosis in macrophages with acute ethanol-exposure.Frontiers in immunology · 2022Article
- Untargeted stable isotope-resolved metabolomics to assess the effect of PI3Kβ inhibition on metabolic pathway activities in a PTEN null breast cancer cell line.Frontiers in molecular biosciences · 2022Article
- Loss of the transcriptional repressor Rev-erbα upregulates metabolism and proliferation in cultured mouse embryonic fibroblasts.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic alterations underlying clear cell renal cell carcinoma (ccRCC) progression include aerobic glycolysis, increased pentose phosphate pathway activity and reduced oxidative phosphorylation. Phosphofructokinase (PFK), a key enzyme of the glycolytic pathway, has L, M, and P isoforms with different tissue distributions. The mRNA level of the platelet isoform of phosphofructokinase (PFKP) is reported to be up-regulated in ccRCC patients. However, it remains unclear whether PFKP plays an important role in promoting aerobic glycolysis and macromolecular biosynthesis to support cell proliferation in ccRCC. Here we found that the up-regulated PFKP became the predominant isoform of PFK in human ccRCC. Suppression of PFKP not only impaired cell proliferation by inducing cell cycle arrest and apoptosis, but also led to decreased glycolysis, pentose phosphate pathway and nucleotide biosynthesis, accompanied by activated tricarboxylic acid cycle in ccRCC cells. Moreover, we found that p53 activation contributed to cell proliferation and metabolic defects induced by PFKP knockdown in ccRCC cells. Furthermore, suppression of PFKP led to reduced ccRCC tumor growth in vivo. Our data indicate that PFKP not only is required for metabolic reprogramming and maintaining cell proliferation, but also may provide us with a valid target for anti-renal cancer pharmaceutical agents.
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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.