Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/49110

TitleCrosstalk between glial and glioblastoma cells triggers the "go-or-grow" phenotype of tumor cells
Author(s)Oliveira, Ana Isabel Ferreira
Anjo, Sandra I.
Castro, Joana Isabel Reis
Serra, Sofia Cristina Cravino
Salgado, A. J.
Manadas, Bruno
Costa, Bruno Marques
KeywordsGlioblastoma
Glial cells
Tumor microenvironment
Secretome
Paracrine effect
Issue date2017
PublisherBioMed Central
JournalCell Communication and Signaling
CitationOliveira, A. I., Anjo, S. I., de Castro, J. V., Serra, S. C., Salgado, A. J., Manadas, B., & Costa, B. M. (2017). Crosstalk between glial and glioblastoma cells triggers the “go-or-grow” phenotype of tumor cells. Cell Communication and Signaling, 15(1), 37
Abstract(s)Background: Glioblastoma (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. Methods: Conditioned 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. Results: The 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. Conclusions: Together, 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.
TypeArticle
URIhttp://hdl.handle.net/1822/49110
DOI10.1186/s12964-017-0194-x
ISSN1478-811X
Publisher versionhttps://biosignaling.biomedcentral.com/articles/10.1186/s12964-017-0194-x
Peer-Reviewedyes
AccessOpen access
Appears in Collections:ICVS - Artigos em Revistas Internacionais com Referee

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