A signature of enhanced lipid metabolism, lipid peroxidation and aldehyde stress in therapy-induced senescence.

ABSTRACT: At their proliferative limit, normal cells arrest and undergo replicative senescence, displaying large cell size, flat morphology, and senescence-associated beta-galactosidase (SA-β-Gal) activity. Normal or tumor cells exposed to genotoxic stress undergo therapy-induced senescence (TIS), displaying a similar phenotype. Senescence is considered a DNA damage response, but cellular heterogeneity has frustrated identification of senescence-specific markers and targets. To explore the senescent cell proteome, we treated tumor cells with etoposide and enriched SA-β-Gal^HI cells by fluorescence-activated cell sorting (FACS). The enriched TIS cells were compared to proliferating or quiescent cells by label-free quantitative LC-MS/MS proteomics and systems analysis, revealin

SUBMITTER: Flor AC 

PROVIDER: S-EPMC5661608 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature