p53/T-antigen complex disruption in T-antigen transformed NIH3T3 fibroblasts exposed to oxidative stress: correlation with the appearance of a Fas/APO-1/CD95 dependent, ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1999-12

AUTHORS

Sandrine Gonin, Chantal Diaz-Latoud, Marie-Jeanne Richard, Mathilde Valeria Ursini, Aude Imbo, Florence Manero, André-Patrick Arrigo

ABSTRACT

Simian Virus 40 Large T-antigen expressed in NIH3T3 cells increases p53 level and interacts with this tumor suppressor to form large nuclear complexes. We show here that T-antigen sensitizes NIH3T3 cells to low doses of the oxidative stress inducer menadione. This oxidant increased p53 accumulation and disrupted p53/T-antigen interaction, but not T-antigen/pRb, T-antigen/Hsc70 and p53/Hsc70 complexes; a phenomenon inhibited by the anti-oxidant N-acetyl-cysteine. Analysis of several p53 downstream gene products revealed that the level of Fas receptor, which was sharply reduced by T-antigen expression, was drastically increased in response to menadione treatment. Menadione also induced a T-antigen dependent cleavage of Fas ligand. Analysis performed with Fas receptor antagonist antibody and metalloproteinases inhibitor revealed that menadione triggers a Fas-dependent death of a fraction of T-antigen expressing cells. This Fas pathway does not activate caspase 8 or 3, probably because of the inhibition induced by T-antigen, and leads to a necrotic cell death which contributes at least in part to the hypersensitivity of T-antigen transformed cells to oxidative stress. More... »

PAGES

1203319

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1203319

DOI

http://dx.doi.org/10.1038/sj.onc.1203319

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1021295840

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10637512


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