ArticleNeuro-oncology2015
Differential regulation of TGF-β-induced, ALK-5-mediated VEGF release by SMAD2/3 versus SMAD1/5/8 signaling in glioblastoma.
Article in Neuro-oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 75 citations in OpenAlex.
- miR‑205: A dual regulator of angiogenesis in health and disease (Review).International journal of molecular medicine · 2026Review
- Non-coding RNAs and angiogenesis in cardiovascular diseases: a comprehensive review.Molecular and cellular biochemistry · 2024Review
- Key Cell-in-Cell Related Genes are Identified by Bioinformatics and Experiments in Glioblastoma.Cancer management and research · 2024Article
- Intracranial Assessment of Androgen Receptor Antagonists in Mice Bearing Human Glioblastoma Implants.International journal of molecular sciences · 2023Article
- Tumor Niches: Perspectives for Targeted Therapies in Glioblastoma.Antioxidants & redox signaling · 2023Review
- Immunological and tumor-intrinsic mechanisms mediate the synergistic growth suppression of experimental glioblastoma by radiotherapy and MET inhibition.Acta neuropathologica communications · 2023Article
- Cell-Type Dependent Regulation of the Electrogenic NaInternational journal of molecular sciences · 2022Article
- CircERBB2IP promotes post-infarction revascularization via the miR-145a-5p/Smad5 axis.Molecular therapy. Nucleic acids · 2022Article
- Uncarboxylated osteocalcin promotes proliferation and metastasis of MDA-MB-231 cells through TGF-β/SMAD3 signaling pathway.BMC molecular and cell biology · 2022Article
- Endoglin aggravates peritoneal fibrosis by regulating the activation of TGF-β/ALK/Smads signaling.Frontiers in pharmacology · 2022Article
- Review
- Synergistic upregulation of ADAMTS4 (aggrecanase-1) by cytokines and its suppression in knee osteoarthritic synovial fibroblasts.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- A tumor-promoting role for soluble TβRIII in glioblastoma.Molecular and cellular biochemistry · 2021Article
- TEM8 marks neovasculogenic tumor-initiating cells in triple-negative breast cancer.Nature communications · 2021Article
- Kallikrein-11, in Association with Coiled-Coil Domain Containing 25, as a Potential Prognostic Marker for Cholangiocarcinoma with Lymph Node Metastasis.Molecules (Basel, Switzerland) · 2021Article
- RETRACTED: Silencing ZEB2 Induces Apoptosis and Reduces Viability in Glioblastoma Cell Lines.Molecules (Basel, Switzerland) · 2021Article
- Alterations in TGFβ signaling during prostate cancer progression.American journal of clinical and experimental urology · 2021Review
- Targeting all transforming growth factor-β isoforms with an Fc chimeric receptor impairs tumor growth and angiogenesis of oral squamous cell cancer.The Journal of biological chemistry · 2020Article
- Association of an anaplastic lymphoma kinase pathway signature with cell de-differentiation, neoadjuvant chemotherapy response, and recurrence risk in breast cancer.Cancer communications (London, England) · 2020Article
- The Involvement of Exosomes in Glioblastoma Development, Diagnosis, Prognosis, and Treatment.Brain sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe transforming growth factor (TGF)-β and vascular endothelial growth factor (VEGF) pathways have a major role in the pathogenesis of glioblastoma, notably immunosuppression, migration, and angiogenesis, but their interactions have remained poorly understood.
methodsWe characterized TGF-β pathway activity in 9 long-term glioma cell lines (LTCs) and 4 glioma-initiating cell lines (GICs) in relation to constitutive and exogenous TGF-β-induced VEGF release. Results were validated using The Cancer Genome Atlas transcriptomics data.
resultsGlioma cells exhibit heterogeneous patterns of constitutive TGF-β pathway activation reflected by phosphorylation not only of SMAD2 and SMAD3 but also of SMAD1/5/8. Constitutive TGF-β pathway activity depends on the type I TGF-β receptor, ALK-5, and accounts for up to 69% of constitutive VEGF release, which is positively regulated by SMAD2/3 and negatively regulated by SMAD1/5/8 signaling in a cell line-specific manner. Exogenous TGF-β induces VEGF release in most cell lines in a SMAD- and ALK-5-dependent manner. There is no correlation between the fold induction of VEGF secretion induced by TGF-β compared with hypoxia. The role of SMAD5 signaling is highly context and cell-line dependent with a VEGF inhibitory effect at low TGF-β and pSMAD2 levels and a stimulatory effect when TGF-β is abundant.
conclusionsTGF-β regulates VEGF release by glioma cells in an ALK-5-dependent manner involving SMAD2, SMAD3, and SMAD1/5/8 signaling. This crosstalk between the TGF-β and VEGF pathways may open up new avenues of biomarker-driven exploratory clinical trials focusing on the microenvironment in glioblastoma.
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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.