ArticleMolecular cancer2024
A positive feedback loop between PFKP and c-Myc drives head and neck squamous cell carcinoma progression.
Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- The RNA-binding protein La/SSB is associated with HNSCC progression and TFAP2C/FSCN1-linked transcriptional regulation.Oncogene · 2026Article
- PFKM acts as a metabolic switch initiating donut-shaped mitochondrial remodeling to promote osteogenesis.International journal of oral science · 2026Article
- HPV16 E7-Associated SERPINB3 Suppression and MYC-Related Epithelial Plasticity in Head and Neck Squamous Cell Carcinoma.Cancers · 2026Article
- rRGD3International journal of molecular sciences · 2026Article
- Review
- IMP metabolic mechanisms and IMPDH targeting strategies in tumor metabolic reprogramming and therapy (Review).International journal of molecular medicine · 2026Review
- TRIM47 Regulates Energy Metabolism via Glycolytic Reprogramming to Drive Hepatocellular Carcinoma Progression and Represents an Efficient Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Metabolic Vulnerabilities as a Therapeutic Target in Breast Cancer.Current oncology (Toronto, Ont.) · 2026Review
- PFKP binding AMOTL1 promotes tumor aerobic glycolysis and epithelial-mesenchymal transition by modulating Hippo pathway in head and neck cancer.Journal of translational internal medicine · 2026Article
- MiR-181a-5p/CDK6 axis attenuates cell proliferation, migration and glycolytic reprogramming in oral squamous cell carcinoma.Cancer cell international · 2026Article
- Diagnostic, Prognostic, and Predictive Molecular Biomarkers in Head and Neck Squamous Cell Carcinoma: A Comprehensive Review.Journal of clinical medicine · 2026Review
- Targeting phosphofructokinase in cancer: integrating natural products for metabolic reprogramming and therapeutic innovation.Frontiers in pharmacology · 2026Review
- Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- Lactylation of PFKP-K688 enhances glycolytic flux and confers cardioprotection in myocardial ischemia.Frontiers in pharmacology · 2026Article
- HMGA1 Activates FGFBP1 Transcription to Enhance Angiogenesis Induction and Tumor Progression via FGF2/FGFR1 Pathway.International journal of biological sciences · 2026Article
- Immunometabolism: crosstalk with tumor metabolism and implications for cancer immunotherapy.Molecular cancer · 2025Review
- Epigenetic Activation of CCDC183-AS1 Promotes Osteoclastogenesis and Prostate Cancer Bone Metastasis Through the FUBP1/LIGHT Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- PKP1 promotes lung cancer by modulating energy metabolism through stabilization of PFKP.Biomarker research · 2025Article
- NNMT-mediated NOncogene · 2025Article
- Phosphofructokinase-1 redefined: a metabolic hub orchestrating cancer hallmarks through multi-dimensional control networks.Journal of translational medicine · 2025Review
Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
backgroundThe aberrant expression of phosphofructokinase-platelet (PFKP) plays a crucial role in the development of various human cancers by modifying diverse biological functions. However, the precise molecular mechanisms underlying the role of PFKP in head and neck squamous cell carcinoma (HNSCC) are not fully elucidated.
methodsWe assessed the expression levels of PFKP and c-Myc in tumor and adjacent normal tissues from 120 HNSCC patients. A series of in vitro and in vivo experiments were performed to explore the impact of the feedback loop between PFKP and c-Myc on HNSCC progression. Additionally, we explored the therapeutic effects of targeting PFKP and c-Myc in HNSCC using Patient-Derived Organoids (PDO), Cell Line-Derived Xenografts, and Patients-Derived Xenografts.
resultsOur findings indicated that PFKP is frequently upregulated in HNSCC tissues and cell lines, correlating with poor prognosis. Our in vitro and in vivo experiments demonstrate that elevated PFKP facilitates cell proliferation, angiogenesis, and metastasis in HNSCC. Mechanistically, PFKP increases the ERK-mediated stability of c-Myc, thereby driving progression of HNSCC. Moreover, c-Myc stimulates PFKP expression at the transcriptional level, thus forming a positive feedback loop between PFKP and c-Myc. Additionally, our multiple models demonstrate that co-targeting PFKP and c-Myc triggers synergistic anti-tumor effects in HNSCC.
conclusionOur study demonstrates the critical role of the PFKP/c-Myc positive feedback loop in driving HNSCC progression and suggests that simultaneously targeting PFKP and c-Myc may be a novel and effective therapeutic strategy for HNSCC.
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