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pubmed-article:8875987pubmed:abstractTextBcl-2 appears to contribute to neoplasia primarily by promoting cell survival, rather than by stimulating cellular proliferation. Bcl-2, and the related protein Bcl-xL, each suppress apoptosis induced by a wide variety of stimuli in many different cell types. Here we report that suppression of apoptosis by Bcl-2 or Bcl-xL markedly elevates the levels of radiation-induced mutations. This enhanced mutagenesis is the result of an increase in mutation frequency (mutations per survivor) together with a moderate increase in viability. Ectopic expression of either Bcl-2 or Bcl-xL enhances radiation mutagenesis in cells with wtp53. Surprisingly, we found that ectopic expression of Bcl-xL also promotes mutagenesis in p53- cells. These results support the hypothesis that apoptosis plays a crucial role in maintaining genomic integrity by selectively eliminating highly mutated cells from the population.lld:pubmed
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pubmed-article:8875987pubmed:articleTitleSuppression of apoptosis by Bcl-2 or Bcl-xL promotes susceptibility to mutagenesis.lld:pubmed
pubmed-article:8875987pubmed:affiliationLife Sciences Division, Lawrence Berkeley National Laboratory, University of California, Berkeley 94720, USA.lld:pubmed
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