Autor: |
Gagliardi Franco, Caruso Riccardo, Arcella Antonietta, Ucci Severine, Porcellini Antonio, De Gregorio Giorgia, Lombari Vincenza, Calogero Antonella, Gulino Alberto, Lanzetta Gaetano, Frati Luigi, Mercola Dan, Ragona Giuseppe |
Jazyk: |
angličtina |
Rok vydání: |
2004 |
Předmět: |
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Zdroj: |
Cancer Cell International, Vol 4, Iss 1, p 1 (2004) |
Druh dokumentu: |
article |
ISSN: |
1475-2867 |
Popis: |
Abstract Background The aim of this work was to investigate in vitro the putative role of EGR-1 in the growth of glioma cells. EGR-1 expression was examined during the early passages in vitro of 17 primary cell lines grown from 3 grade III and from 14 grade IV malignant astrocytoma explants. The explanted tumors were genetically characterized at the p53, MDM2 and INK4a/ARF loci, and fibronectin expression and growth characteristics were examined. A recombinant adenovirus overexpressing EGR-1 was tested in the primary cell lines. Results Low levels of EGR-1 protein were found in all primary cultures examined, with lower values present in grade IV tumors and in cultures carrying wild-type copies of p53 gene. The levels of EGR-1 protein were significantly correlated to the amount of intracellular fibronectin, but only in tumors carrying wild-type copies of the p53 gene (R = 0,78, p = 0.0082). Duplication time, plating efficiency, colony formation in agarose, and contact inhibition were also altered in the p53 mutated tumor cultures compared to those carrying wild-type p53. Growth arrest was achieved in both types of tumor within 1–2 weeks following infection with a recombinant adenovirus overexpressing EGR-1 but not with the control adenovirus. Conclusions Suppression of EGR-1 is a common event in gliomas and in most cases this is achieved through down-regulation of gene expression. Expression of EGR-1 by recombinant adenovirus infection almost completely abolishes the growth of tumor cells in vitro, regardless of the mutational status of the p53 gene. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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