ArticleNeuro-oncology2020
CCL5 of glioma-associated microglia/macrophages regulates glioma migration and invasion via calcium-dependent matrix metalloproteinase 2.
Article in Neuro-oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.
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Who cites it
104 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.
- Glioblastoma invasion patterns from a clinical perspective-a systematic review.Neurosurgical review · 2024Pooled it
- The intersection of chemokine signaling with the hallmarks of cancer in glioblastoma.Journal of neuro-oncology · 2026Review
- Attract to kill: Exploring the potential of motility trapping as a novel treatment strategy for high-grade gliomas.Neuro-oncology · 2026Review
- Predicting glioma survival and extracellular matrix remodeling through MRI radiogenomics.Cell reports. Medicine · 2026Article
- M2-like GAMs secreting CSTA drive glioblastoma progression via the ITGB4-TGFB1 feedback axis.Journal of translational medicine · 2026Article
- SERPINA3 facilitates malignant progression and remodels tumor immune microenvironment in glioma.Biochemistry and biophysics reports · 2026Article
- Cancer neuroscience: signaling pathways and new therapeutic strategies for cancer.Signal transduction and targeted therapy · 2026Review
- 3D heterotypic models of glioblastoma reveal the impact of microglia on cellular organization and the production of a distinct secretome.Scientific reports · 2026Article
- Nested ecosystems theory for conceptualizing brain tumors.Disease models & mechanisms · 2026Review
- Diversity and function of tumor-associated macrophages in brain metastases: mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- Decoding the cGAS-STING-eosinophils predictive and natural therapeutic molecular signature in burn injury progression and keloid formation: insights from artificial intelligence-driven multiomics.Frontiers in surgery · 2026Article
- Review
- Natural killer cell dysfunction in glioma: from immune evasion to immunotherapy.Frontiers in immunology · 2026Review
- Brain metastasis from non-small cell lung cancer: crosstalk between cancer cells and tumor microenvironment components.Experimental & molecular medicine · 2025Review
- H3K36me3-Guided mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Advances in Cellular Immune Theranostic Approaches for Glioblastoma: Current Trends and Future Directions.Cancer innovation · 2025Review
- Glioblastoma-associated macrophages in glioblastoma: from their function and mechanism to therapeutic advances.Cancer gene therapy · 2025Review
- Ribosomal protein S3A (RPS3A), as a transcription regulator of colony-stimulating factor 1 (CSF1), promotes glioma progression through regulating the recruitment and autophagy-mediated M2 polarization of tumor-associated macrophages.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Review
- Mapping glioma progression: single-cell RNA sequencing illuminates cell-cell interactions and immune response variability.Discover oncology · 2025Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioma-associated microglia/macrophages (GAMs) comprise macrophages of peripheral origin and brain-intrinsic microglia, which support tumor progression. Chemokine C-C ligand 5 (CCL5) is an inflammatory mediator produced by immune cells and is involved in tumor growth and migration in several cancers, including glioma. However, the mechanisms detailing how CCL5 facilitates glioma invasion remain largely unresolved.
methodsGlioma migration and invasion were determined by wound healing, transwell assay, and 3D µ-slide chemotaxis assay. The expression levels of CCL5, CD68, matrix metalloproteinase 2 (MMP2), phosphorylated Ca2+/calmodulin-dependent protein kinase II (p-CaMKII), p-Akt, and phosphorylated proline-rich tyrosine kinase 2 were determined by cytokine array, quantitative PCR, western blot, or immunohistochemistry. Zymography and intracellular calcium assays were used to analyze MMP2 activity and intracellular calcium levels, respectively.
resultsCCL5 modulated the migratory and invasive activities of human glioma cells in association with MMP2 expression. In response to CCL5, glioma cells underwent a synchronized increase in intracellular calcium levels and p-CaMKII and p-Akt expression levels. CCL5-directed glioma invasion and increases in MMP2 were suppressed after inhibition of p-CaMKII. Glioma cells tended to migrate toward GAM-conditioned media activated by granulocyte-macrophage colony-stimulating factor (GM-CSF) in which CCL5 was abundant. This homing effect was associated with MMP2 upregulation, and could be ameliorated either by controlling intracellular and extracellular calcium levels or by CCL5 antagonism. Clinical results also revealed the associations between CCL5 and GAM activation.
conclusionOur results suggest that modulation of glioma CaMKII may restrict the effect of CCL5 on glioma invasion and could be a potential therapeutic target for alleviating glioma growth.
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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.