ArticleNeuro-oncology2018
VEGF-C sustains VEGFR2 activation under bevacizumab therapy and promotes glioblastoma maintenance.
Article in Neuro-oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 86 citations in OpenAlex.
- Immunohistochemistry study of tumor vascular normalization and anti-angiogenic effects of sunitinib versus bevacizumab prior to dose-dense doxorubicin/cyclophosphamide chemotherapy in HER2-negative breast cancer.Breast cancer research and treatment · 2022Trial
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- Silencing of lncRNA HOTAIR Using Eyedrops as a Potential Treatment for Diabetes-Associated Retinal Dysregulation and Dysfunction.Investigative ophthalmology & visual science · 2026Article
- Anlotinib Combined with Programmed Death-1/Programmed Death-Ligand 1 Inhibitor 9 Hydrochloride Suppresses Colorectal Cancer Progression by Inducing Neovascularization and Reprogramming the Tumor Immune Microenvironment in MSS Murine Model.ImmunoTargets and therapy · 2026Article
- Article
- Bispecific receptor decoy proteins block ocular neovascularization via simultaneous blockade of vascular endothelial growth factor A and C.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Angiogenesis and targeted therapy in the tumour microenvironment: From basic to clinical practice.Clinical and translational medicine · 2025Review
- Blocking Tumoral Angiogenesis VEGF/VEGFR Pathway: Bevacizumab-20 Years of Therapeutic Success and Controversy.Cancers · 2025Review
- Article
- Breaking the premetastatic niche barrier: the role of endothelial cells and therapeutic strategies.Theranostics · 2025Review
- Treatment mechanism and research progress of bevacizumab for glioblastoma.American journal of cancer research · 2025Review
- In Silico Approach to Model Heat Distribution of Magnetic Hyperthermia in the Tumoral and Healthy Vascular Network Using Tumor-on-a-Chip to Evaluate Effective Therapy.Pharmaceutics · 2024Article
- Bevacizumab-Based Therapies in Malignant Tumors-Real-World Data on Effectiveness, Safety, and Cost.Cancers · 2024Article
- Vascular Endothelial Growth Factor C and D Signaling Pathways as Potential Targets for the Treatment of Neovascular Age-Related Macular Degeneration: A Narrative Review.Ophthalmology and therapy · 2024Review
- Connecting the Dots: The Cerebral Lymphatic System as a Bridge Between the Central Nervous System and Peripheral System in Health and Disease.Aging and disease · 2024Review
- Article
- Anti-angiogenic Potential of Trans-chalcone in anCardiovascular & hematological agents in medicinal chemistry · 2024Article
- Advancing precision medicine in gliomas through single-cell sequencing: unveiling the complex tumor microenvironment.Frontiers in cell and developmental biology · 2024Review
- In vivo antiangiogenic effect of nimbolide, trans-chalcone and piperine for use against glioblastoma.BMC cancer · 2023Article
- DeepAutoGlioma: a deep learning autoencoder-based multi-omics data integration and classification tools for glioma subtyping.BioData mining · 2023Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glioblastoma ranks among the most lethal cancers, with current therapies offering only palliation. Paracrine vascular endothelial growth factor (VEGF) signaling has been targeted using anti-angiogenic agents, whereas autocrine VEGF/VEGF receptor 2 (VEGFR2) signaling is poorly understood. Bevacizumab resistance of VEGFR2-expressing glioblastoma cells prompted interrogation of autocrine VEGF-C/VEGFR2 signaling in glioblastoma. Methods: Autocrine VEGF-C/VEGFR2 signaling was functionally investigated using RNA interference and exogenous ligands in patient-derived xenograft lines and primary glioblastoma cell cultures in vitro and in vivo. VEGF-C expression and interaction with VEGFR2 in a matched pre- and post-bevacizumab treatment cohort were analyzed by immunohistochemistry and proximity ligation assay. Results: VEGF-C was expressed by patient-derived xenograft glioblastoma lines, primary cells, and matched surgical specimens before and after bevacizumab treatment. VEGF-C activated autocrine VEGFR2 signaling to promote cell survival, whereas targeting VEGF-C expression reprogrammed cellular transcription to attenuate survival and cell cycle progression. Supporting potential translational significance, targeting VEGF-C impaired tumor growth in vivo, with superiority to bevacizumab treatment. Conclusions: Our results demonstrate VEGF-C serves as both a paracrine and an autocrine pro-survival cytokine in glioblastoma, promoting tumor cell survival and tumorigenesis. VEGF-C permits sustained VEGFR2 activation and tumor growth, where its inhibition appears superior to bevacizumab therapy in improving tumor control.
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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.