期刊
AGING CELL
卷 13, 期 5, 页码 946-950出版社
WILEY-BLACKWELL
DOI: 10.1111/acel.12234
关键词
replicative aging; senescence; DNA damage; telomerase expression; cell cycle
资金
- Glenn Center for Research on Aging
- Human Frontier Science Program
- Japan Society for the Promotion of Science
- NIH NRSA T32 Fellowship [5T32CA009370-29]
- Salk Institute Cancer Center Core Grant [P30CA014195]
- NIH [R01GM087476, R01CA174942]
- John Sabo Trust
- Fritz B. Burns Foundation
- Highland Street Foundation
Replicative senescence is a fundamental tumor-suppressive mechanism triggered by telomere erosion that results in a permanent cell cycle arrest. To understand the impact of telomere shortening on gene expression, we analyzed the transcriptome of diploid human fibroblasts as they progressed toward and entered into senescence. We distinguished novel transcription regulation due to replicative senescence by comparing senescence-specific expression profiles to profiles from cells arrested by DNA damage or serum starvation. Only a small specific subset of genes was identified that was truly senescence-regulated and changes in gene expression were exacerbated from presenescent to senescent cells. The majority of gene expression regulation in replicative senescence was shown to occur due to telomere shortening, as exogenous telomerase activity reverted most of these changes.
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