The radioprotective effect of the 24 kDa FGF-2 isoform in HeLa cells is related to an increased expression and activity ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2002-09

AUTHORS

Isabelle Ader, Catherine Muller, Jacques Bonnet, Gilles Favre, Elizabeth Cohen-Jonathan, Bernard Salles, Christine Toulas

ABSTRACT

We previously reported that overexpression of the 24 kDa basic fibroblast factor (or FGF-2) isoform provides protection from the cytotoxic effect of ionizing radiation (IR). DNA double-strand breaks (DSB), the IR-induced lethal lesions, are mainly repaired in human cells by non-homologous end joining system (NHEJ). NHEJ reaction is dependent on the DNA-PK holoenzyme (composed of a regulatory sub-unit, Ku, and a catalytic sub-unit, DNA-PKcs) that assembles at sites of DNA damage. We demonstrated here that the activity of DNA-PK was increased by twofold in two independent radioresistant cell lines, HeLa 3A and CAPAN A3, over expressing the 24 kDa FGF-2. This increase was associated with an overexpression of the DNA-PKcs without modification of Ku expression or activity. This overexpression was due to an up-regulation of the DNA-PKcs gene transcription by the 24 kDa FGF-2 isoform. Finally, HeLa 3A cells exhibited the hallmarks of phenotypic changes associated with the overexpression of an active DNA-PKcs. Indeed, a faster repair rate of DSB and sensitization to IR by wortmannin was observed in these cells. Our results represent the characterization of a new mechanism of control of DNA repair and radioresistance in human tumor cells dependent on the overproduction of the 24 kDa FGF-2 isoform. More... »

PAGES

1205838

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1205838

DOI

http://dx.doi.org/10.1038/sj.onc.1205838

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1042884536

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12226750


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