ArticleBritish journal of cancer2022
Glycometabolic reprogramming-mediated proangiogenic phenotype enhancement of cancer-associated fibroblasts in oral squamous cell carcinoma: role of PGC-1α/PFKFB3 axis.
Article in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 34 citations in OpenAlex.
- Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens.Poultry science · 2026Article
- Chorus line in oral squamous cell carcinoma: How stromal and immune players orchestrate tumor progression (Review).International journal of molecular medicine · 2026Review
- USP5 promotes glycolysis in cervical cancer by stabilizing FOXM1.American journal of cancer research · 2026Article
- HMGA1 Activates FGFBP1 Transcription to Enhance Angiogenesis Induction and Tumor Progression via FGF2/FGFR1 Pathway.International journal of biological sciences · 2026Article
- Unraveling the impact of cancer-associated fibroblasts on lymphatic metastasis of head and neck squamous cell carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Role of metabolic reprogramming of cancer‑associated fibroblasts in tumor development and progression (Review).International journal of oncology · 2025Review
- MiR-1293 modulates PPARGC1A to promote proliferation and metastasis of oral carcinoma cells.Journal of molecular histology · 2025Article
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- Nano-drug delivery strategies affecting cancer-associated fibroblasts to reduce tumor metastasis.Acta pharmaceutica Sinica. B · 2025Review
- Role of PGC-1α in the proliferation and metastasis of malignant tumors.Journal of molecular histology · 2025Review
- Fibroblast-immune crosstalk in oral squamous cell carcinoma: from tumor promotion to immune evasion.Frontiers in immunology · 2025Review
- Research progress on cancer-associated fibroblasts in osteosarcoma.Oncology research · 2025Review
- NNMT switches the proangiogenic phenotype of cancer-associated fibroblasts via epigenetically regulating ETS2/VEGFA axis.Oncogene · 2024Article
- Enhanced lipid biosynthesis in oral squamous cell carcinoma cancer-associated fibroblasts contributes to tumor progression: Role of IL8/AKT/p-ACLY axis.Cancer science · 2024Article
- Heterogeneity of cancer-associated fibroblasts and tumor-promoting roles in head and neck squamous cell carcinoma.Frontiers in molecular biosciences · 2024Review
- Decoding tumor-fibrosis interplay: mechanisms, impact on progression, and innovative therapeutic strategies.Frontiers in pharmacology · 2024Review
- From metabolism to malignancy: the multifaceted role of PGC1α in cancer.Frontiers in oncology · 2024Review
- Comparative clinical significance and biological roles of PFKFB family members in oral squamous cell carcinoma.Cancer cell international · 2023Article
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8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundAngiogenesis is a key rate-limiting step in the process of tumour progression. Cancer-associated fibroblasts (CAFs), the most abundant component OSCC stroma, play important roles in pro-angiogenesis. Recently, the stroma "reverse Warburg effect" was proposed, and PFKFB3 has been brought to the forefront as a metabolic enzyme regulating glycometabolism. However, it remains unclear whether glycometabolism reprogramming is involved in promoting the angiogenesis of CAFs.
methodsCAFs and paracancerous fibroblasts (PFs) were isolated from OSCC and adjacent tissues. We detected the pro-angiogenesis and glycometabolism phenotype of three pairs of fibroblasts. Targeted blockage of PFKFB3 or activation of PGC-1α signal was used to investigate the effect of glycolysis on regulating angiogenesis of CAFs in vitro and vivo.
resultsCAFs exhibited metabolic reprogramming and enhanced proangiogenic phenotype compared with PFs. Inhibition of PFKFB3-dependent glycolysis impaired proangiogenic factors (VEGF-A, PDGF-C and MMP9) expression in CAFs. Furthermore, CAFs proangiogenic phenotype was regulated by glycometabolism through the PGC-1α/PFKFB3 axis. Consistently, PGC-1α overexpression or PFKFB3 knockdown in CAFs slowed down tumour development by reducing tumour angiogenesis in the xenograft model.
conclusionCAFs of OSCC are characterised with glycometabolic reprogramming and enhanced proangiogenic phenotypes. Our findings suggest that activating PGC-1α signalling impairs proangiogenic phenotype of CAFs by blocking PFKFB3-driven glycolysis.
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