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Loss of p21(Sdi1) expression in senescent cells after DNA damage accompanied with increase of miR-93 expression and reduced p53 interaction with p21(Sdi1) gene promoter

Authors
Choi, OR; Lim, IK
Citation
Biochemical and biophysical research communications, 407(2):406-411, 2011
Journal Title
Biochemical and biophysical research communications
ISSN
0006-291X1090-2104
Abstract
To answer what is a critical event for higher incidence of tumor development in old than young individuals, primary culture of human diploid fibroblasts were employed and DNA damage was induced by doxorubicin or X-ray irradiation. Response to the damage was different between young and old cells; loss of p21(sdi1) expression in spite of p53(S¹⁵) activation in old cells along with [³H]thymidine and BrdU incorporation, but not in young cells. The phenomenon was confirmed by other tissue fibroblasts obtained from different donor ages. Induction of miR-93 expression and reduced p53 binding to p21 gene promoter account for loss of p21(sdi1) expression in senescent cells after DNA damage, suggesting a mechanism of in vivo carcinogenesis in aged tissue without repair arrest.
MeSH terms
AdultAgedCell Aging/*geneticsCell Transformation, Neoplastic/*genetics/pathologyCells, CulturedChild, PreschoolCyclin-Dependent Kinase Inhibitor p21/*genetics*DNA DamageFibroblasts/drug effects/pathology/radiation effects*Gene Expression Regulation, NeoplasticHumansMaleMicroRNAs/*geneticsMiddle AgedPromoter Regions, GeneticTumor Suppressor Protein p53/*metabolismYoung Adult
DOI
10.1016/j.bbrc.2011.03.038
PMID
21402054
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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임, 인경
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