ArticleFrontiers in molecular neuroscience2018
Fibronectin Promotes the Malignancy of Glioma Stem-Like Cells Via Modulation of Cell Adhesion, Differentiation, Proliferation and Chemoresistance.
Article in Frontiers in molecular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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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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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
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Glioma Stem Cells as Promoter of Glioma Progression: A Systematic Review of Molecular Pathways and Targeted Therapies.International journal of molecular sciences · 2024Pooled it
- Microglia in diffuse midline glioma contribute to extracellular matrix remodelling and cancer cell invasion.Cell death & disease · 2026Article
- Harnessing innate immunity against glioblastoma microenvironment.Frontiers in immunology · 2025Review
- Glioma actively orchestrate a self-advantageous extracellular matrix to promote recurrence and progression.BMC cancer · 2024Review
- Epithelial CEBPD activates fibronectin and enhances macrophage adhesion in renal ischemia-reperfusion injury.Cell death discovery · 2024Article
- Biosensor-Enhanced Organ-on-a-Chip Models for Investigating Glioblastoma Tumor Microenvironment Dynamics.Sensors (Basel, Switzerland) · 2024Review
- The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance.Frontiers in oncology · 2024Review
- Cancer stem cells and their niche in cancer progression and therapy.Cancer cell international · 2023Review
- Engineering the glioblastoma microenvironment with bioactive nanoparticles for effective immunotherapy.RSC advances · 2023Review
- Engineered In Vitro Tumor Model Recapitulates Molecular Signatures of Invasion in Glioblastoma.ACS materials Au · 2023Article
- Extracellular matrix-derived mechanical force governs breast cancer cell stemness and quiescence transition through integrin-DDR signaling.Signal transduction and targeted therapy · 2023Article
- Review
- Article
- Glioblastoma Microenvironment and Invasiveness: New Insights and Therapeutic Targets.International journal of molecular sciences · 2023Review
- Pancreatic cancer cells upregulate LPAR4 in response to isolation stress to promote an ECM-enriched niche and support tumour initiation.Nature cell biology · 2023Article
- Re-Sensitizing Cancer Stem Cells to Conventional Chemotherapy Agents.International journal of molecular sciences · 2023Review
- Proteomics reveals differentially regulated pathways when comparing grade 2 and 4 astrocytomas.PloS one · 2023Article
- Culturing and Imaging Glioma Stem Cells in 3D Collagen Matrices.Current protocols · 2023Article
- Laminin-5, Fibronectin, and Type IV Collagen as Potential Biomarkers of Brain Glioma Malignancy.Biomedicines · 2022Article
- Collagen Remodeling along Cancer Progression Providing a Novel Opportunity for Cancer Diagnosis and Treatment.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma stem-like cells (GSCs) are regarded as the sources of oncogenesis, recurrence, invasion and chemoresistance in malignant gliomas. Growing evidence suggests that the microenvironment surrounding GSCs interacts with tumor cells to influence biological behavior; however, the functional mechanisms involved are still unclear. In the present study, we investigated the modulation of GSCs triggered by fibronectin (FN), a main component of the extracellular matrix (ECM), in terms of cell adhesion, differentiation, proliferation and chemoresistance. We demonstrated that pre-coated FN prompted increased adherence by GSCs, with increased matrix metallopeptidases (MMPs)-2 and -9 expression, in a concentration-dependent manner. Decreases in sox-2 and nestin levels, and increased levels of glial fibrillary acidic protein (GFAP) and β-tubulin were also found in GSCs, indicating cell differentiation driven by FN. Further investigation revealed that FN promoted cell growth, as demonstrated by the elevation of Ki-67, with the activation of p-ERK1/2 and cyclin D1 also evident. In addition, FN suppressed p53-mediated apoptosis and upregulated P-glycoprotein expression, making GSCs more chemoresistant to alkylating agents such as carmustine. In contrast, this effect was reversed by an integrin inhibitor, cilengitide. Activation of the focal adhesion kinase/paxillin/AKT signaling pathway was involved in the modulation of GSCs by FN. Focusing on the interactions between tumor cells and the ECM may be an encouraging aspect of research on novel chemotherapeutic therapies in future.
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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.