ArticleCell communication and signaling : CCS2017
Crosstalk between glial and glioblastoma cells triggers the "go-or-grow" phenotype of tumor cells.
Article in Cell communication and signaling : CCS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Tracing the origins of glioblastoma by investigating the role of gliogenic and related neurogenic genes/signaling pathways in GBM development: a systematic review.World journal of surgical oncology · 2022Pooled it
- Heterogenous Model of Temozolomide Resistance in Glioblastoma Reveals Phenotypic Shifts in Drug Response and Migratory Potential.Advanced nanobiomed research · 2026Article
- 3D heterotypic models of glioblastoma reveal the impact of microglia on cellular organization and the production of a distinct secretome.Scientific reports · 2026Article
- Unraveling the Effects and Characteristics of Proliferating Tumor and Cytotoxic T Cells in Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Unraveling Glioblastoma: TME Implication and Gene Therapy Advances.Current gene therapy · 2025Review
- Biosensor-Enhanced Organ-on-a-Chip Models for Investigating Glioblastoma Tumor Microenvironment Dynamics.Sensors (Basel, Switzerland) · 2024Review
- Review
- Cellular Conversations in Glioblastoma Progression, Diagnosis and Treatment.Cellular and molecular neurobiology · 2023Review
- The tumor micro-environment in pediatric glioma: friend or foe?Frontiers in immunology · 2023Review
- An overview of glioblastoma multiforme and temozolomide resistance: can LC-MS-based proteomics reveal the fundamental mechanism of temozolomide resistance?Frontiers in oncology · 2023Review
- Effects of Long-Term Temozolomide Treatment on Glioblastoma and Astrocytoma WHO Grade 4 Stem-like Cells.International journal of molecular sciences · 2022Article
- Understanding glioblastoma invasion using physically-guided neural networks with internal variables.PLoS computational biology · 2022Article
- The Hallmarks of Glioblastoma: Heterogeneity, Intercellular Crosstalk and Molecular Signature of Invasiveness and Progression.Biomedicines · 2022Review
- Chronic Stress Does Not Influence the Survival of Mouse Models of Glioblastoma.Frontiers in oncology · 2022Article
- Recent advances in the use of CRISPR/Cas for understanding the early development of molecular gaps in glial cells.Frontiers in cell and developmental biology · 2022Review
- Integrative analysis of CBR1 as a prognostic factor associated with IDH-mutant glioblastoma in the Chinese population.American journal of translational research · 2022Article
- Spatial Dissection of Invasive Front from Tumor Mass Enables Discovery of Novel microRNA Drivers of Glioblastoma Invasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Connexin 43 and Sonic Hedgehog Pathway Interplay in Glioblastoma Cell Proliferation and Migration.Biology · 2021Article
- Hans Joachim Scherer: an under-recognized pioneer of glioma research in Belgium.Acta neurologica Belgica · 2021Review
- Systems-Level Proteomics Evaluation of Microglia Response to Tumor-Supportive Anti-Inflammatory Cytokines.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma (GBM), the most malignant primary brain tumor, leads to poor and unpredictable clinical outcomes. Recent studies showed the tumor microenvironment has a critical role in regulating tumor growth by establishing a complex network of interactions with tumor cells. In this context, we investigated how GBM cells modulate resident glial cells, particularly their paracrine activity, and how this modulation can influence back on the malignant phenotype of GBM cells.
methodsConditioned media (CM) of primary mouse glial cultures unexposed (unprimed) or exposed (primed) to the secretome of GL261 GBM cells were analyzed by proteomic analysis. Additionally, these CM were used in GBM cells to evaluate their impact in glioma cell viability, migration capacity and activation of tumor-related intracellular pathways.
resultsThe proteomic analysis revealed that the pre-exposure of glial cells to CM from GBM cells led to the upregulation of several proteins related to inflammatory response, cell adhesion and extracellular structure organization within the secretome of primed glial cells. At the functional levels, CM derived from unprimed glial cells favored an increase in GBM cell migration capacity, while CM from primed glial cells promoted cells viability. These effects on GBM cells were accompanied by activation of particular intracellular cancer-related pathways, mainly the MAPK/ERK pathway, which is a known regulator of cell proliferation.
conclusionsTogether, our results suggest that glial cells can impact on the pathophysiology of GBM tumors, and that the secretome of GBM cells is able to modulate the secretome of neighboring glial cells, in a way that regulates the "go-or-grow" phenotypic switch of GBM cells.
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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.