ArticleCell death and differentiation2018
BMP9 counteracts the tumorigenic and pro-angiogenic potential of glioblastoma.
Article in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Characteristics of vasculogenic mimicry and tumour to endothelial transdifferentiation in human glioblastoma: a systematic review.BMC cancer · 2023Pooled it
- Bmpr2 Loss in the Vascular Endothelium Enhances Neoangiogenesis and Growth of Lung Metastatic Lesions in a Mouse Model of Breast Cancer.Journal of cellular biochemistry · 2025Article
- Connexin hemichannel blockade by abEC1.1 disrupts glioblastoma progression, suppresses invasiveness, and reduces hyperexcitability in preclinical models.Cell communication and signaling : CCS · 2025Article
- Endothelial transdifferentiation of glioma stem cells: a literature review.Acta neuropathologica communications · 2025Review
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Cancer cell stiffening via CoQNature communications · 2024Article
- The TGF-β Family in Glioblastoma.International journal of molecular sciences · 2024Review
- BMP signaling in cancer stemness and differentiation.Cell regeneration (London, England) · 2023Review
- Article
- Hydrogen Sulphide-Based Therapeutics for Neurological Conditions: Perspectives and Challenges.Neurochemical research · 2023Review
- A novel matrine derivative, WM130, inhibits activation and movement of human hepatic stellate LX-2 cells by targeting cofilin 1.Cytotechnology · 2022Article
- Correlation of the prognostic value of FNDC4 in glioblastoma with macrophage polarization.Cancer cell international · 2022Article
- Cofilin Acts as a Booster for Progression of Malignant Tumors Represented by Glioma.Cancer management and research · 2022Review
- The Dual Effect of the BMP9-ALK1 Pathway in Blood Vessels: An Opportunity for Cancer Therapy Improvement?Cancers · 2021Review
- The role of Serpina3n in the reversal effect of ATRA on dexamethasone-inhibited osteogenic differentiation in mesenchymal stem cells.Stem cell research & therapy · 2021Article
- Single-cell analyses reveal YAP/TAZ as regulators of stemness and cell plasticity in Glioblastoma.Nature cancer · 2021Article
- Novel Pathways for Targeting Tumor Angiogenesis in Metastatic Breast Cancer.Frontiers in oncology · 2021Review
- EndothelialArteriosclerosis, thrombosis, and vascular biology · 2020Article
- EB1-dependent long survival of glioblastoma-grafted mice with the oral tubulin-binder BAL101553 is associated with inhibition of tumor angiogenesis.Oncotarget · 2020Article
- A novel circular RNA circENTPD7 contributes to glioblastoma progression by targeting ROS1.Cancer cell international · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is a highly vascularized and aggressive brain tumor, with a strong ability to disseminate and invade the surrounding parenchyma. In addition, a subpopulation of GBM stem cells has been reported to possess the ability to transdifferentiate into tumor-derived endothelial cells (TDECs), supporting the resistance to anti-angiogenic treatments of newly formed blood vessels. Bone Morphogenetic Protein 9 (BMP9) is critically involved in the processes of cancer cell differentiation, invasion and metastasis, representing a potential tool in order to impair the intrinsic GBM aggressiveness. Here we demonstrate that BMP9 is able to trigger the activation of SMADs in patient-derived GBM cells, and to strongly inhibit proliferation and invasion by reducing the activation of PI3K/AKT/MAPK and RhoA/Cofilin pathways, respectively. Intriguingly, BMP9 treatment is sufficient to induce a strong differentiation of GBM stem-like cells and to significantly counteract the already reported process of GBM cell transdifferentiation into TDECs not only in in vitro mimicked TDEC models, but also in vivo in orthotopic xenografts in mice. Additionally, we describe a strong BMP9-mediated inhibition of the whole angiogenic process engaged during GBM tumor formation. Based on these results, we believe that BMP9, by acting at multiple levels against GBM cell aggressiveness, can be considered a promising candidate, to be further developed, for the future therapeutic management of GBM.
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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.