A Comparison of Oncogene-induced Senescence and Replicative Senescence: Implications for Tumor Suppression and Aging

Overview

Journal Age (Dordr)

Publisher Springer

Specialty Geriatrics

Date 2014 Mar 21

PMID 24647599

Citations 31

Authors

David M Nelson

Tony McBryan

Jessie C Jeyapalan

John M Sedivy

Peter D Adams

Affiliations

Soon will be listed here.

Abstract

Cellular senescence is a stable proliferation arrest associated with an altered secretory pathway, the senescence-associated secretory phenotype. However, cellular senescence is initiated by diverse molecular triggers, such as activated oncogenes and shortened telomeres, and is associated with varied and complex physiological endpoints, such as tumor suppression and tissue aging. The extent to which distinct triggers activate divergent modes of senescence that might be associated with different physiological endpoints is largely unknown. To begin to address this, we performed gene expression profiling to compare the senescence programs associated with two different modes of senescence, oncogene-induced senescence (OIS) and replicative senescence (RS [in part caused by shortened telomeres]). While both OIS and RS are associated with many common changes in gene expression compared to control proliferating cells, they also exhibit substantial differences. These results are discussed in light of potential physiological consequences, tumor suppression and aging.

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