Literature DB >> 3892307

Overproduction of p53 antigen makes established cells highly tumorigenic.

D Eliyahu, D Michalovitz, M Oren.   

Abstract

The p53 cellular tumour antigen, long known to be overproduced in a variety of neoplastically transformed cells, was recently shown to be directly involved in transformation. Thus, p53 can complement activated Ha-ras in transforming secondary rat embryo fibroblasts into grossly altered, tumorigenic cells. Moreover, p53 can also be shown to possess immortalizing activity. Our previous results indicated, however, that the contribution of p53 to the transformation was not synonymous with immortalization, suggesting that the two activities of the protein are probably separable. We demonstrate here that this is indeed the case, as overproduction of p53 in an established cell line, while not causing gross morphological changes, endows these cells with an overt tumorigenic potential. Furthermore, the tumorigenic efficiency of such cell lines may be correlated with the extent of p53 over-production.

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Year:  1985        PMID: 3892307     DOI: 10.1038/316158a0

Source DB:  PubMed          Journal:  Nature        ISSN: 0028-0836            Impact factor:   49.962


  60 in total

1.  Middle T antigen activation of signal transduction pathways does not overcome p53-mediated growth arrest.

Authors:  J Doherty; R Freund
Journal:  J Virol       Date:  1999-09       Impact factor: 5.103

2.  Regions and activities of simian virus 40 T antigen that cooperate with an activated ras oncogene in transforming primary rat embryo fibroblasts.

Authors:  Tina M Beachy; Sara L Cole; Jane F Cavender; Mary J Tevethia
Journal:  J Virol       Date:  2002-04       Impact factor: 5.103

3.  Identification of a minimal transforming domain of p53: negative dominance through abrogation of sequence-specific DNA binding.

Authors:  E Shaulian; A Zauberman; D Ginsberg; M Oren
Journal:  Mol Cell Biol       Date:  1992-12       Impact factor: 4.272

4.  Replication of an E1B 55-kilodalton protein-deficient adenovirus (ONYX-015) is restored by gain-of-function rather than loss-of-function p53 mutants.

Authors:  Byron Hann; Allan Balmain
Journal:  J Virol       Date:  2003-11       Impact factor: 5.103

5.  Resistance to oncogenic transformation in revertant R1 of human ras-transformed NIH 3T3 cells.

Authors:  N Kuzumaki; Y Ogiso; A Oda; H Fujita; H Suzuki; C Sato; L Müllauer
Journal:  Mol Cell Biol       Date:  1989-05       Impact factor: 4.272

6.  Mutation is required to activate the p53 gene for cooperation with the ras oncogene and transformation.

Authors:  P Hinds; C Finlay; A J Levine
Journal:  J Virol       Date:  1989-02       Impact factor: 5.103

7.  Stabilization of the p53 transformation-related protein in mouse fibrosarcoma cell lines: effects of protein sequence and intracellular environment.

Authors:  O Halevy; A Hall; M Oren
Journal:  Mol Cell Biol       Date:  1989-08       Impact factor: 4.272

8.  A mutant p53 protein is required for maintenance of the transformed phenotype in cells transformed with p53 plus ras cDNAs.

Authors:  G P Zambetti; D Olson; M Labow; A J Levine
Journal:  Proc Natl Acad Sci U S A       Date:  1992-05-01       Impact factor: 11.205

Review 9.  The first 30 years of p53: growing ever more complex.

Authors:  Arnold J Levine; Moshe Oren
Journal:  Nat Rev Cancer       Date:  2009-10       Impact factor: 60.716

10.  Modulation of immortalizing properties of human papillomavirus type 16 E7 by p53 expression.

Authors:  T Crook; C Fisher; K H Vousden
Journal:  J Virol       Date:  1991-01       Impact factor: 5.103

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