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Glioblastoma cells inhibit astrocytic p53-expression favoring cancer malignancy.
Biasoli, D; Sobrinho, M F; da Fonseca, A C C; de Matos, D G; Romão, L; de Moraes Maciel, R; Rehen, S K; Moura-Neto, V; Borges, H L; Lima, F R S.
Afiliação
  • Biasoli D; Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • Sobrinho MF; Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • da Fonseca AC; Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • de Matos DG; Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • Romão L; Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • de Moraes Maciel R; 1] Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil [2] D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil.
  • Rehen SK; 1] Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil [2] D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil.
  • Moura-Neto V; Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • Borges HL; Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • Lima FR; Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Oncogenesis ; 3: e123, 2014 Oct 20.
Article em En | MEDLINE | ID: mdl-25329722
The tumor microenvironment has a dynamic and usually cancer-promoting function during all tumorigenic steps. Glioblastoma (GBM) is a fatal tumor of the central nervous system, in which a substantial number of non-tumoral infiltrated cells can be found. Astrocytes neighboring these tumor cells have a particular reactive phenotype and can enhance GBM malignancy by inducing aberrant cell proliferation and invasion. The tumor suppressor p53 has a potential non-cell autonomous function by modulating the expression of secreted proteins that influence neighbor cells. In this work, we investigated the role of p53 on the crosstalk between GBM cells and astrocytes. We show that extracellular matrix (ECM) from p53(+/-) astrocytes is richer in laminin and fibronectin, compared with ECM from p53(+/+) astrocytes. In addition, ECM from p53(+/-) astrocytes increases the survival and the expression of mesenchymal markers in GBM cells, which suggests haploinsufficient phenotype of the p53(+/-) microenvironment. Importantly, conditioned medium from GBM cells blocks the expression of p53 in p53(+/+) astrocytes, even when DNA was damaged. These results suggest that GBM cells create a dysfunctional microenvironment based on the impairment of p53 expression that in turns exacerbates tumor endurance.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Oncogenesis Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Oncogenesis Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos