Journal
EMBO REPORTS
Volume 8, Issue 5, Pages 497-503Publisher
WILEY
DOI: 10.1038/sj.embor.7400937
Keywords
telomere; DNA damage; p53; senescence
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Funding
- NCI NIH HHS [R01 CA129037, P01 CA34936-20, P30 CA016672, CA016672, P01 CA034936] Funding Source: Medline
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Dysfunctional telomeres induce p53-dependent cellular senescence and apoptosis, but it is not known which function is more important for tumour suppression in vivo. We used the p53(R172P) knock-in mouse, which is unable to induce apoptosis but retains intact cell-cycle arrest and cellular senescence pathways, to show that spontaneous tumorigenesis is potently repressed in Terc(-/-)p53(R172P) mice. Tumour suppression is accompanied by global induction of p53, p21 and the senescence marker senescence-associated-beta-galactosidase. By contrast, cellular senescence was unable to suppress chemically induced skin carcinomas. These results indicate that suppression of spontaneous tumorigenesis by dysfunctional telomeres requires the activation of the p53-dependent cellular senescence pathway.
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