ArticleBiomaterials2014
A composite hydrogel platform for the dissection of tumor cell migration at tissue interfaces.
Article in Biomaterials, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 48 citations in OpenAlex.
- The Size of Glioblastoma Spheroids Influences Patterns of Invasion and Temozolomide Efficacy.Tissue engineering. Part C, Methods · 2026Article
- Mechanotransduction in glioma stem cell fate determination: from niche mechanics to therapeutic vulnerability and state plasticity.Frontiers in cell and developmental biology · 2026Review
- Size-dependent invasion and therapeutic phenotype of 42MGBA glioblastoma spheroids.bioRxiv : the preprint server for biology · 2025Article
- The mechanism and potential therapeutic target of piezo channels in pain.Frontiers in pain research (Lausanne, Switzerland) · 2024Review
- A deep learning-based pipeline for analyzing the influences of interfacial mechanochemical microenvironments on spheroid invasion using differential interference contrast microscopic images.Materials today. Bio · 2023Article
- Exploring New Dimensions of Tumor Heterogeneity: The Application of Single Cell Analysis to Organoid-Based 3D In Vitro Models.Advanced healthcare materials · 2023Review
- HYDRHA: Hydrogels of hyaluronic acid. New biomedical approaches in cancer, neurodegenerative diseases, and tissue engineering.Materials today. Bio · 2022Review
- Nuclear plasticity increases susceptibility to damage during confined migration.PLoS computational biology · 2020Article
- Extravascular gelation shrinkage-derived internal stress enables tumor starvation therapy with suppressed metastasis and recurrence.Nature communications · 2019Article
- Dissecting and rebuilding the glioblastoma microenvironment with engineered materials.Nature reviews. Materials · 2019Article
- Mechanisms of invasion and motility of high-grade gliomas in the brain.Molecular biology of the cell · 2018Review
- A 3D topographical model of parenchymal infiltration and perivascular invasion in glioblastoma.APL bioengineering · 2018Article
- Role of Microenvironment in Glioma Invasion: What We Learned from In Vitro Models.International journal of molecular sciences · 2018Review
- Three-dimensional hydrogel is suitable for targeted investigation of amoeboid migration of glioma cells.Molecular medicine reports · 2018Article
- The Influence of Hyaluronic Acid and Glioblastoma Cell Coculture on the Formation of Endothelial Cell Networks in Gelatin Hydrogels.Advanced healthcare materials · 2017Article
- Integrating the glioblastoma microenvironment into engineered experimental models.Future science OA · 2017Review
- Engineered Models of Confined Cell Migration.Annual review of biomedical engineering · 2016Review
- Mechanical confinement triggers glioma linear migration dependent on formin FHOD3.Molecular biology of the cell · 2016Article
- Actomyosin stress fiber mechanosensing in 2D and 3D.F1000Research · 2016Review
- Deconstructing the role of the ECM microenvironment on drug efficacy targeting MAPK signaling in a pre-clinical platform for cutaneous melanoma.Biomaterials · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma multiforme (GBM), the most prevalent primary brain cancer, is characterized by diffuse infiltration of tumor cells into brain tissue, which severely complicates surgical resection and contributes to tumor recurrence. The most rapid mode of tissue infiltration occurs along blood vessels or white matter tracts, which represent topological interfaces thought to serve as "tracks" that speed cell migration. Despite this observation, the field lacks experimental paradigms that capture key features of these tissue interfaces and allow reductionist dissection of mechanisms of this interfacial motility. To address this need, we developed a culture system in which tumor cells are sandwiched between a fibronectin-coated ventral surface representing vascular basement membrane and a dorsal hyaluronic acid (HA) surface representing brain parenchyma. We find that inclusion of the dorsal HA surface induces formation of adhesive complexes and significantly slows cell migration relative to a free fibronectin-coated surface. This retardation is amplified by inclusion of integrin binding peptides in the dorsal layer and expression of CD44, suggesting that the dorsal surface slows migration through biochemically specific mechanisms rather than simple steric hindrance. Moreover, both the reduction in migration speed and assembly of dorsal adhesions depend on myosin activation and the stiffness of the ventral layer, implying that mechanochemical feedback directed by the ventral layer can influence adhesive signaling at the dorsal surface.
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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.