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Survive or thrive: tradeoff strategy for cellular senescence

Title
Survive or thrive: tradeoff strategy for cellular senescence
Authors
Park, SC[Park, Sang Chul]
DGIST Authors
Park, SC[Park, Sang Chul]
Issue Date
2017-06
Citation
Experimental and Molecular Medicine, 49
Type
Article
Article Type
Review
Keywords
Apoptosis ResistanceCaveolin Scaffolding DomainDown RegulationFocal Adhesion KinaseHuman Diploid FibroblastsNuclear Pore ComplexPremature SenescenceProtein KinasesReceptor Mediated EndocytosisTranscription Factor SP1
ISSN
1226-3613
Abstract
Aging-dependent cellular behaviors toward extrinsic stress are characterized by the confined localization of certain molecules to either nuclear or perinuclear regions. Although most growth factors can activate downstream signaling in aging cells, they do not in fact have any impact on the cells because the signals cannot reach their genetic targets in the nucleus. For the same reason, varying apoptotic stress factors cannot stimulate the apoptotic pathway in senescent cells. Thus, the operation of a functional nuclear barrier in an aging-dependent manner has been investigated. To elucidate the mechanism for this process, the housekeeping transcription factor Sp1 was identified as a general regulator of nucleocytoplasmic trafficking (NCT) genes, including various nucleoporins, importins, exportins and Ran GTPase cycle-related genes. Interestingly, the posttranslational modification of Sp1 is readily influenced by extrinsic stress, including oxidative and metabolic stress. The decrease in SP1 O-GlcNAcylation under oxidative stress or during replicative senescence makes it susceptible to proteosomal degradation, resulting in defective NCT functions and leading to nuclear barrier formation. The operation of the nuclear barrier in aging provides a fundamental mechanism for cellular protection against stress and promotes survival at the expense of growth via stress-sensitive transcriptional control.
URI
http://hdl.handle.net/20.500.11750/4161
DOI
10.1038/emm.2017.94
Publisher
NATURE PUBLISHING GROUP
Files:
There are no files associated with this item.
Collection:
New BiologyETC1. Journal Articles


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