ArticleNature cell biology2014
Profilin-1 phosphorylation directs angiocrine expression and glioblastoma progression through HIF-1α accumulation.
Article in Nature cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
61 citing papers in PubMed, 95 citations in OpenAlex.
- Computational Phosphosite-Specific Network Analysis of YES1 Y426 Reveals Cancer-Associated Phosphorylation Patterns.Proteomes · 2026Article
- RAGE Axis in the Pathogenesis and Treatment of CNS Neurodegeneration in Long-Term Hyperglycemia.International journal of molecular sciences · 2026Review
- Small molecule intervention of actin-binding protein profilin1 reduces tumor angiogenesis in renal cell carcinoma.bioRxiv : the preprint server for biology · 2025Article
- Von Hippel-Lindau/Hypoxia Inducible Factor Axis in Glioblastoma.International journal of molecular sciences · 2025Review
- Decoding the lactylation-immune link in calcific aortic valve disease: a comprehensive bioinformatics approach.Human genomics · 2025Article
- Integrated spectroscopic and morphological analyses reveal cellular shifts in gene-silenced melanoma CSCs.Scientific reports · 2025Article
- Machine learning-based integration develops a hypoxia-derived signature for improving outcomes in glioma.iScience · 2025Article
- CD71-Mediated Effects of Soluble Vasorin on Tumor Progression, Angiogenesis and Immunosuppression.International journal of molecular sciences · 2025Article
- Overexpression of miR-328-3p Inhibits Epithelial-Mesenchymal Transition in Prostate Cancer by Downregulating PFN1.Applied biochemistry and biotechnology · 2025Article
- Extracellular Vesicles Carrying Tenascin-C are Clinical Biomarkers and Improve Tumor-Derived DNA Analysis in Glioblastoma Patients.ACS nano · 2025Article
- FLASH radiation reprograms lipid metabolism and macrophage immunity and sensitizes medulloblastoma to CAR-T cell therapy.Nature cancer · 2025Article
- Lactylation-related gene signatures identify glioma molecular subtypes with prognostic, immunological, and therapeutic implications.Frontiers in oncology · 2025Article
- FNDC4 alleviates cardiac ischemia/reperfusion injury through facilitating HIF1α-dependent cardiomyocyte survival and angiogenesis in male mice.Nature communications · 2024Article
- Understanding the Significance of Hypoxia-Inducible Factors (HIFs) in Glioblastoma: A Systematic Review.Cancers · 2024Review
- FBXO22 promotes glioblastoma malignant progression by mediating VHL ubiquitination and degradation.Cell death discovery · 2024Article
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- Small-molecule toosendanin reverses macrophage-mediated immunosuppression to overcome glioblastoma resistance to immunotherapy.Science translational medicine · 2023Article
- BAL Proteomic Signature of Lung Adenocarcinoma in IPF Patients and Its Transposition in Serum Samples for Less Invasive Diagnostic Procedures.International journal of molecular sciences · 2023Article
- USP33 deubiquitinates and stabilizes HIF-2alpha to promote hypoxia response in glioma stem cells.The EMBO journal · 2022Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The tumour vascular microenvironment supports tumorigenesis not only by supplying oxygen and diffusible nutrients but also by secreting soluble factors that promote tumorigenesis. Here we identify a feedforward mechanism in which endothelial cells (ECs), in response to tumour-derived mediators, release angiocrines driving aberrant vascularization and glioblastoma multiforme (GBM) progression through a hypoxia-independent induction of hypoxia-inducible factor (HIF)-1α. Phosphorylation of profilin-1 (Pfn-1) at Tyr 129 in ECs induces binding to the tumour suppressor protein von Hippel-Lindau (VHL), and prevents VHL-mediated degradation of prolyl-hydroxylated HIF-1α, culminating in HIF-1α accumulation even in normoxia. Elevated HIF-1α induces expression of multiple angiogenic factors, leading to vascular abnormality and tumour progression. In a genetic model of GBM, mice with an EC-specific defect in Pfn-1 phosphorylation exhibit reduced tumour angiogenesis, normalized vasculature and improved survival. Moreover, EC-specific Pfn-1 phosphorylation is associated with tumour aggressiveness in human glioma. These findings suggest that targeting Pfn-1 phosphorylation may offer a selective strategy for therapeutic intervention of malignant solid tumours.
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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.