Response of Ewing tumor cells to forced and activated p53 expression View Full Text


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Article Info

DATE

2003-05-22

AUTHORS

Heinrich Kovar, Sarka Pospisilova, Gunhild Jug, Dieter Printz, Helmut Gadner

ABSTRACT

The EWS-FLI1 transcription factor is consistently expressed in 85% of Ewing tumors (EFT). In heterologous cells, EWS-FLI1 induces p53-dependent cell cycle arrest or apoptosis. It has been speculated that the p53 tumor suppressor pathway may be generally compromised in EFT despite only rare p53 mutations. In order to test for functional integrity of this pathway, we have investigated a series of EFT cell lines that differ from each other with respect to their endogenous p53 and INK4A gene status for their response to ectopic p53 expression and to stimulation of endogenous p53 activity by X-ray treatment. Significant interindividual and intratumoral variations in the apoptotic propensity of EFT cell lines to transient expression of ectopic p53 were observed, which was independent of the level of p53 expression. In cell lines with a low apoptotic incidence, apoptosis was delayed and the surviving fraction showed a prolonged growth arrest. Complete resistance to p53-induced apoptosis in two cell lines established from the same patient was associated with a high BCL2/BAX ratio and low levels of APAF1. Sensitivity to X-rays showed a trend towards a higher apoptotic rate in wild-type (wt) p53 expressing than in p53 mutant cells. However, one wt p53-expressing EFT cell line was completely refractory to irradiation-stimulated cell death despite high apoptotic responsiveness to ectopic p53. No difference in Ser15 phosphorylation and the transcriptional activation of p53 targets was observed in wt p53 EFT cell lines irrespective of the induction of cell death or growth arrest. All together, our results demonstrate that despite significant variability in the outcome, cell death or cell cycle arrest, the p53 downstream pathway and the DNA damage signaling pathway are functionally intact in EFT. More... »

PAGES

3193-3204

References to SciGraph publications

  • 1997-05. Regulation of p53 stability by Mdm2 in NATURE
  • 1997-05. Mdm2 promotes the rapid degradation of p53 in NATURE
  • 1999-09-01. An association between viral genes and human oncogenic alterations: The adenovirus E1A induces the Ewing tumor fusion transcript EWS–FLI1 in NATURE MEDICINE
  • 1999-01-28. p73 at chromosome 1p36.3 is lost in advanced stage neuroblastoma but its mutation is infrequent in ONCOGENE
  • 1997-10-30. Among genes involved in the RB dependent cell cycle regulatory cascade, the p16 tumor suppressor gene is frequently lost in the Ewing family of tumors in ONCOGENE
  • 1998-02. Effects of p53 mutants derived from lung carcinomas on the p53-responsive element (p53RE) of the MDM2 gene in BRITISH JOURNAL OF CANCER
  • 2000-08-24. Characterization of distinct consecutive phases in non-genotoxic p53-induced apoptosis of Ewing tumor cells and the rate-limiting role of caspase 8 in ONCOGENE
  • 1997-01. Inhibition of EWS-FLI-1 fusion protein with antisense oligodeoxynucleotides in JOURNAL OF NEURO-ONCOLOGY
  • 1999-07. Genomic organization of the human caspase-9 gene on Chromosome 1p36.1-p36.3 in MAMMALIAN GENOME
  • 1999-12-13. The role of the E6-p53 interaction in the molecular pathogenesis of HPV in ONCOGENE
  • 2001-10-11. Loss of p16 pathways stabilizes EWS/FLI1 expression and complements EWS/FLI1 mediated transformation in ONCOGENE
  • 1995. The PITSLRE protein kinase family in PROGRESS IN CELL CYCLE RESEARCH
  • 1998-05-14. Human tumor-derived p53 proteins exhibit binding site selectivity and temperature sensitivity for transactivation in a yeast-based assay in ONCOGENE
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/sj.onc.1206391

    DOI

    http://dx.doi.org/10.1038/sj.onc.1206391

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1007451007

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/12761489


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