ArticleMolecular medicine reports2021
Platelet isoform of phosphofructokinase promotes aerobic glycolysis and the progression of non‑small cell lung cancer.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Review
- Glycolysis-related genes for bladder cancer: A Mendelian randomization analysis.Biochemistry and biophysics reports · 2026Article
- PFKP in malignant tumors: bridging metabolic reprogramming, post-translational modifications, and the immunosuppressive microenvironment.Frontiers in cell and developmental biology · 2026Review
- Catabolic rewiring in cancer impacts dietary interventions.Communications biology · 2025Review
- The role of the transcription factor PATZ1 in tumorigenesis and metabolic regulation.Journal of cancer research and clinical oncology · 2025Review
- Phosphofructokinase-1 redefined: a metabolic hub orchestrating cancer hallmarks through multi-dimensional control networks.Journal of translational medicine · 2025Review
- The Emerging Roles of Metabolic Reprogramming in Non-Small Cell Lung Cancer Progression.Frontiers in bioscience (Landmark edition) · 2025Review
- Exploring the relationship between hypoxia in lung adenocarcinoma and tumor microenvironment immune cell infiltration.Discover oncology · 2025Article
- Phosphofructokinase-1 in Cancer: A Promising Target for Diagnosis and Therapy.Recent patents on anti-cancer drug discovery · 2025Review
- A positive feedback loop between PFKP and c-Myc drives head and neck squamous cell carcinoma progression.Molecular cancer · 2024Article
- PFKP silencing suppresses tumor growth via the AXL-MET axis.International journal of biological sciences · 2024Article
- Increased epithelial mTORC1 activity in chronic rhinosinusitis with nasal polyps.bioRxiv : the preprint server for biology · 2023Article
- A high-throughput screening campaign against PFKFB3 identified potential inhibitors with novel scaffolds.Acta pharmacologica Sinica · 2023Article
- Proteotranscriptomic Discrimination of Tumor and Normal Tissues in Renal Cell Carcinoma.International journal of molecular sciences · 2023Article
- Phosphofructokinase Platelet Overexpression Accelerated Colorectal Cancer Cell Growth and Motility.Journal of Cancer · 2023Article
- PFKP: More than phosphofructokinase.Advances in cancer research · 2023Review
- Essential role of aerobic glycolysis in epithelial-to-mesenchymal transition during carcinogenesis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- How Phosphofructokinase-1 Promotes PI3K and YAP/TAZ in Cancer: Therapeutic Perspectives.Cancers · 2022Article
- Targeting glycolysis in non-small cell lung cancer: Promises and challenges.Frontiers in pharmacology · 2022Review
- Characteristics of hypoxic tumor microenvironment in non-small cell lung cancer, involving molecular patterns and prognostic signature.Translational lung cancer research · 2021Article
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3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The platelet isoform of phosphofructokinase (PFKP) is a rate‑limiting enzyme involved in glycolysis that serves an important role in various types of cancer. The aim of the present study was to explore the specific regulatory relationship between PFKP and non‑small cell lung cancer (NSCLC) progression. PFKP expression in NSCLC tissues and corresponding adjacent tissues was detected using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and immunohistochemical analysis. PFKP expression in human bronchial epithelial cells (16HBE) and NSCLC cells (H1299, H23 and A549) was also detected using RT‑qPCR. Cell proliferation was detected by Cell Counting Kit‑8 and colony formation assays. Transwell invasion and wound healing assays, and flow cytometry were used to detect cell invasion, migration and apoptosis, respectively. The expression levels of glycolysis‑associated enzymes (hexokinase‑2, lactate dehydrogenase A and glucose transporter‑1), epithelial‑mesenchymal transition‑related proteins (N‑cadherin, vimentin and E‑cadherin) and apoptosis‑related proteins (caspase‑3 and B‑cell lymphoma‑2) were detected by western blotting. Glucose uptake, lactate production and the adenosine trisphosphate/adenosine diphosphate ratio were measured using the corresponding kits. The results of the present study demonstrated that PFKP expression was upregulated in NSCLC tissues and cells, and PFKP expression was related to lymph node metastasis and histological grade. In addition, overexpression of PFKP inhibited cell apoptosis, and promoted proliferation, migration, invasion and glycolysis of H1299 cells, whereas knockdown of PFKP had the opposite effects. In conclusion, PFKP inhibited cell apoptosis, and promoted proliferation, migration, invasion and glycolysis of NSCLC cells; these findings may lay the foundation for novel treatments of NSCLC.
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