ArticlePloS one2017
Neuropilin-1 modulates TGFβ signaling to drive glioblastoma growth and recurrence after anti-angiogenic therapy.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 45 citations in OpenAlex.
- TGF-β-induced Tregs release extracellular vesicles that modulate CD4+ T-cell proliferation and phenotype in a Nrp1-dependent manner.ImmunoHorizons · 2026Article
- Modulation of endothelial-to-mesenchymal transition via NRP-1 targeting with melittin attenuates pulmonary fibrosis.Materials today. Bio · 2026Article
- Silencing MALAT1 represses pathological progression, inflammation, and vascular smooth muscle cell phenotype switching by regulating the SEMA3C-mediated Smad pathway in intracranial aneurysms.Frontiers in cellular neuroscience · 2026Article
- Article
- Therapeutic targeting of TGF-β in lung cancer.The FEBS journal · 2025Review
- Neuropilin-1: A Multifaceted Target for Cancer Therapy.Current oncology (Toronto, Ont.) · 2025Review
- Transforming growth factor-β receptors: versatile mechanisms of ligand activation.Acta pharmacologica Sinica · 2024Review
- New Salicylanilide Derivatives and Their Peptide Conjugates as Anticancer Compounds: Synthesis, Characterization, andACS omega · 2024Article
- Mechanisms of Acquired Resistance to Anti-VEGF Therapy for Neovascular Eye Diseases.Investigative ophthalmology & visual science · 2023Review
- Neuropilin (NRPs) Related Pathological Conditions and Their Modulators.International journal of molecular sciences · 2022Review
- Article
- The contribution of neuropilin-1 in the stability of CD4Immunity, inflammation and disease · 2022Article
- Neuropilin-1 is over-expressed in claudin-low breast cancer and promotes tumor progression through acquisition of stem cell characteristics and RAS/MAPK pathway activation.Breast cancer research : BCR · 2022Article
- Neuropilin-1 modulates the 3D invasive properties of glioblastoma stem-like cells.Frontiers in cell and developmental biology · 2022Article
- Identification of Hub Genes and Key Pathways Associated with Anti-Biomolecules · 2021Article
- Neuropilin-1: A Key Protein to Consider in the Progression of Pediatric Brain Tumors.Frontiers in oncology · 2021Review
- Efficacy and safety of bevacizumab combined with temozolomide in the treatment of recurrent malignant gliomas and its influence on serum tumor markers.American journal of translational research · 2021Article
- Ablation of neuropilin-1 improves the therapeutic response in conventional drug-resistant glioblastoma multiforme.Oncogene · 2020Article
- Autophagy as a mechanism for anti-angiogenic therapy resistance.Seminars in cancer biology · 2020Review
- αvβ8 integrin adhesion and signaling pathways in development, physiology and disease.Journal of cell science · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is a rapidly progressive brain cancer that exploits the neural microenvironment, and particularly blood vessels, for selective growth and survival. Anti-angiogenic agents such as the vascular endothelial growth factor-A (VEGF-A) blocking antibody bevacizumab yield short-term benefits to patients due to blood vessel regression and stabilization of vascular permeability. However, tumor recurrence is common, and this is associated with acquired resistance to bevacizumab. The mechanisms that drive acquired resistance and tumor recurrence in response to anti-angiogenic therapy remain largely unknown. Here, we report that Neuropilin-1 (Nrp1) regulates GBM growth and invasion by balancing tumor cell responses to VEGF-A and transforming growth factor βs (TGFβs). Nrp1 is expressed in GBM cells where it promotes TGFβ receptor internalization and signaling via Smad transcription factors. GBM that recur after bevacizumab treatment show down-regulation of Nrp1 expression, indicating that altering the balance between VEGF-A and TGFβ signaling is one mechanism that promotes resistance to anti-angiogenic agents. Collectively, these data reveal that Nrp1 plays a critical role in balancing responsiveness to VEGF-A versus TGFβ to regulate GBM growth, progression, and recurrence after anti-vascular therapy.
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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.