ArticleOncotarget2017
Tumor-associated mesenchymal stem-like cells provide extracellular signaling cue for invasiveness of glioblastoma cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- The Interplay of Microtubules with Mitochondria-ER Contact Sites (MERCs) in Glioblastoma.Biomolecules · 2022Pooled it
- Extracellular Matrix Remodeling in Tumors: Forces Beyond Fibroblasts.Cancer research · 2026Article
- Complement-Targeted Therapies in Glioblastoma: A Systematic Review.Biomedicines · 2026Review
- The Extracellular Matrix, the Silent 'Architect' of Glioma.Biomedicines · 2026Review
- Restoring the glioblastoma tumor microenvironment by targeting C5a with the antagonist W54011.Scientific reports · 2025Article
- The Role of TIM-3 in Glioblastoma Progression.Cells · 2025Review
- Benign non-immune cells in tumor microenvironment.Frontiers in immunology · 2025Review
- Revisiting the role of mesenchymal stromal cells in cancer initiation, metastasis and immunosuppression.Experimental hematology & oncology · 2024Review
- Glioblastoma-Associated Mesenchymal Stem/Stromal Cells and Cancer-Associated Fibroblasts: Partners in Crime?International journal of molecular sciences · 2024Review
- Nanomedicine Strategies for Targeting Tumor Stroma.Cancers · 2023Review
- Mesenchymal Stem-Like Cells Derived from the Ventricle More Effectively Enhance Invasiveness of Glioblastoma Than Those Derived from the Tumor.Yonsei medical journal · 2023Article
- Biomimetic Hydrogels in the Study of Cancer Mechanobiology: Overview, Biomedical Applications, and Future Perspectives.Gels (Basel, Switzerland) · 2022Review
- Glioblastoma-educated mesenchymal stem-like cells promote glioblastoma infiltration via extracellular matrix remodelling in the tumour microenvironment.Clinical and translational medicine · 2022Article
- Molecular Mechanisms and Clinical Challenges of Glioma Invasion.Brain sciences · 2022Review
- Bioengineered Models to Study Microenvironmental Regulation of Glioblastoma Metabolism.Journal of neuropathology and experimental neurology · 2021Review
- Antitumor effect of 4MU on glioblastoma cells is mediated by senescence induction and CD44, RHAMM and p-ERK modulation.Cell death discovery · 2021Article
- Influence of the Amount of Fresh Specimen on the Isolation of Tumor Mesenchymal Stem-Like Cells from High-Grade Glioma.Yonsei medical journal · 2021Article
- Glioma-Associated Stromal Cells Stimulate Glioma Malignancy by Regulating the Tumor Immune Microenvironment.Frontiers in oncology · 2021Article
- The Relationship Between Mesenchymal Stem Cells and Tumor Dormancy.Frontiers in cell and developmental biology · 2021Review
- Cross talk between mesenchymal and glioblastoma stem cells: Communication beyond controversies.Stem cells translational medicine · 2020Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyaluronic acid (HA) is abundant in tumor microenvironment and closely associated with invasiveness of glioblastoma (GBM) cells. However, the cellular mechanism underlying HA-rich microenvironment in GBM remains unexplored. Here, we show that tumor-associated mesenchymal stem-like cells (tMSLCs) contribute to abundance of hyaluronic acid (HA) in tumor microenvironment through HA synthase-2 (HAS2) induction, and thereby enhances invasiveness of GBM cells. In an autocrine manner, C5a secreted by tMSLCs activated ERK MAPK for HAS2 induction in tMSLCs. Importantly, HA acted as a signaling ligand of its cognate receptor RHAMM for intracellular signaling activation underlying invasiveness of GBM cells. Taken together, our study suggests that tMSLCs contribute to HA-rich proinvasive ECM microenvironment in 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.