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Downregulation of Polo-Like Kinase 1 Induces Cellular Senescence in Human Primary Cells Through a p53-Dependent Pathway

Polo-like kinase 1 (PLK1) plays a key role in various stages of mitosis from entry into M phase to exit from mitosis. However, its role in cellular senescence remains to be determined. Therefore, the effects of PLK1 on cellular senescence in human primary cells were investigated. We found that expre... Full description

Journal Title: Journals of Gerontology Series A: Biomedical Sciences and Medical Sciences 2013, Vol. 68(10), pp.1145-1156
Main Author: Kim, Hee - Jin
Other Authors: Cho, Jung Hee , Kim, Jae - Ryong
Format: Electronic Article Electronic Article
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Subjects:
P53
ID: ISSN: 1079-5006 ; E-ISSN: 1758-535X ; DOI: 10.1093/gerona/glt017
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recordid: oxford10.1093/gerona/glt017
title: Downregulation of Polo-Like Kinase 1 Induces Cellular Senescence in Human Primary Cells Through a p53-Dependent Pathway
format: Article
creator:
  • Kim, Hee - Jin
  • Cho, Jung Hee
  • Kim, Jae - Ryong
subjects:
  • Polo - Like Kinase 1
  • Cellular Senescence
  • P53
  • Human Primary Cells.
ispartof: Journals of Gerontology Series A: Biomedical Sciences and Medical Sciences, 2013, Vol. 68(10), pp.1145-1156
description: Polo-like kinase 1 (PLK1) plays a key role in various stages of mitosis from entry into M phase to exit from mitosis. However, its role in cellular senescence remains to be determined. Therefore, the effects of PLK1 on cellular senescence in human primary cells were investigated. We found that expression of PLK1 decreased in human dermal fibroblasts and human umbilical vein endothelial cells under replicative senescence and premature senescence induced by adriamycin. PLK1 knockdown with PLK1 small interfering RNAs in young cells induced premature senescence. In contrast, upregulation of PLK1 in old cells partially reversed senescence phenotypes. Cellular senescence by PLK1 inhibition was observed in p16 knockdown cells but not in p53 knockdown cells. Our data suggest that PLK1 repression might result in cellular senescence in human primary cells via a p53-dependent pathway.
language:
source:
identifier: ISSN: 1079-5006 ; E-ISSN: 1758-535X ; DOI: 10.1093/gerona/glt017
fulltext: fulltext
issn:
  • 1079-5006
  • 10795006
  • 1758-535X
  • 1758535X
url: Link


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subjectPolo - Like Kinase 1 ; Cellular Senescence ; P53 ; Human Primary Cells.
descriptionPolo-like kinase 1 (PLK1) plays a key role in various stages of mitosis from entry into M phase to exit from mitosis. However, its role in cellular senescence remains to be determined. Therefore, the effects of PLK1 on cellular senescence in human primary cells were investigated. We found that expression of PLK1 decreased in human dermal fibroblasts and human umbilical vein endothelial cells under replicative senescence and premature senescence induced by adriamycin. PLK1 knockdown with PLK1 small interfering RNAs in young cells induced premature senescence. In contrast, upregulation of PLK1 in old cells partially reversed senescence phenotypes. Cellular senescence by PLK1 inhibition was observed in p16 knockdown cells but not in p53 knockdown cells. Our data suggest that PLK1 repression might result in cellular senescence in human primary cells via a p53-dependent pathway.
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descriptionPolo-like kinase 1 (PLK1) plays a key role in various stages of mitosis from entry into M phase to exit from mitosis. However, its role in cellular senescence remains to be determined. Therefore, the effects of PLK1 on cellular senescence in human primary cells were investigated. We found that expression of PLK1 decreased in human dermal fibroblasts and human umbilical vein endothelial cells under replicative senescence and premature senescence induced by adriamycin. PLK1 knockdown with PLK1 small interfering RNAs in young cells induced premature senescence. In contrast, upregulation of PLK1 in old cells partially reversed senescence phenotypes. Cellular senescence by PLK1 inhibition was observed in p16 knockdown cells but not in p53 knockdown cells. Our data suggest that PLK1 repression might result in cellular senescence in human primary cells via a p53-dependent pathway.
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abstractPolo-like kinase 1 (PLK1) plays a key role in various stages of mitosis from entry into M phase to exit from mitosis. However, its role in cellular senescence remains to be determined. Therefore, the effects of PLK1 on cellular senescence in human primary cells were investigated. We found that expression of PLK1 decreased in human dermal fibroblasts and human umbilical vein endothelial cells under replicative senescence and premature senescence induced by adriamycin. PLK1 knockdown with PLK1 small interfering RNAs in young cells induced premature senescence. In contrast, upregulation of PLK1 in old cells partially reversed senescence phenotypes. Cellular senescence by PLK1 inhibition was observed in p16 knockdown cells but not in p53 knockdown cells. Our data suggest that PLK1 repression might result in cellular senescence in human primary cells via a p53-dependent pathway.
pubOxford University Press
doi10.1093/gerona/glt017
date2013-03-10