Inhibition of cell growth by EGR-1 in human primary cultures from malignant glioma

Antonella Calogero, Vincenza Lombari, Giorgia De Gregorio, Antonio Porcellini, Severine Ucci, Antonietta Arcella, Riccardo Caruso, Franco Maria Gagliardi, Alberto Gulino, Gaetano Lanzetta, Luigi Frati, Dan Mercola, Giuseppe Ragona

Research output: Contribution to journalArticle

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.

Original languageEnglish
Article number1
JournalCancer Cell International
Volume4
DOIs
Publication statusPublished - Jan 7 2004

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Glioma
p53 Genes
Growth
Adenoviridae
Neoplasms
Fibronectins
Contact Inhibition
Adenoviridae Infections
Cell Line
Gene Expression Regulation
Glioblastoma
Sepharose
Proteins
Down-Regulation
Infection
In Vitro Techniques

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Calogero, A., Lombari, V., De Gregorio, G., Porcellini, A., Ucci, S., Arcella, A., ... Ragona, G. (2004). Inhibition of cell growth by EGR-1 in human primary cultures from malignant glioma. Cancer Cell International, 4, [1]. https://doi.org/10.1186/1475-2867-4-1

Inhibition of cell growth by EGR-1 in human primary cultures from malignant glioma. / Calogero, Antonella; Lombari, Vincenza; De Gregorio, Giorgia; Porcellini, Antonio; Ucci, Severine; Arcella, Antonietta; Caruso, Riccardo; Gagliardi, Franco Maria; Gulino, Alberto; Lanzetta, Gaetano; Frati, Luigi; Mercola, Dan; Ragona, Giuseppe.

In: Cancer Cell International, Vol. 4, 1, 07.01.2004.

Research output: Contribution to journalArticle

Calogero, A, Lombari, V, De Gregorio, G, Porcellini, A, Ucci, S, Arcella, A, Caruso, R, Gagliardi, FM, Gulino, A, Lanzetta, G, Frati, L, Mercola, D & Ragona, G 2004, 'Inhibition of cell growth by EGR-1 in human primary cultures from malignant glioma', Cancer Cell International, vol. 4, 1. https://doi.org/10.1186/1475-2867-4-1
Calogero, Antonella ; Lombari, Vincenza ; De Gregorio, Giorgia ; Porcellini, Antonio ; Ucci, Severine ; Arcella, Antonietta ; Caruso, Riccardo ; Gagliardi, Franco Maria ; Gulino, Alberto ; Lanzetta, Gaetano ; Frati, Luigi ; Mercola, Dan ; Ragona, Giuseppe. / Inhibition of cell growth by EGR-1 in human primary cultures from malignant glioma. In: Cancer Cell International. 2004 ; Vol. 4.
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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.",
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AU - Ucci, Severine

AU - Arcella, Antonietta

AU - Caruso, Riccardo

AU - Gagliardi, Franco Maria

AU - Gulino, Alberto

AU - Lanzetta, Gaetano

AU - Frati, Luigi

AU - Mercola, Dan

AU - Ragona, Giuseppe

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AB - 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.

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