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Journal of Biochemistry Advance Access originally published online on March 11, 2009
Journal of Biochemistry 2009 146(1):87-93; doi:10.1093/jb/mvp046
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© The Authors 2009. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved

Protein Kinase C {delta} Plays a Key Role in Cellular Senescence Programs of Human Normal Diploid Cells

Yoshinori Katakura1,2,3,*,{dagger}, Miyako Udono2,{dagger}, Kazuyuki Katsuki3, Hisaya Nishide2, Yukiko Tabira2, Takahiro Ikei2, Makiko Yamashita1, Tsukasa Fujiki1 and Sanetaka Shirahata1,2,3

1Department of Genetic Resources Technology, Faculty of Agriculture; 2Graduate School of Bioresources and Bioenvironmental Sciences; and 3Graduate School of Systems Life Sciences, Kyushu University, Fukuoka 812-8581, Japan

*To whom correspondence should be addressed. Tel: +81-92-642-3050; Fax: +81-92-642-3050; E-mail: katakura{at}grt.kyushu-u.ac.jp

Received November 19, 2008; Accepted March 5, 2009


  Abstract

In the present study, we clarified that transforming growth factor β (TGF-β) induces cellular senescence in human normal diploid cells, TIG-1, and identified protein kinase Cs (PKCs) as downstream mediators of TGF-β-induced cellular senescence. Among PKCs, we showed that PKC-{delta} induced cellular senescence in TIG-1 cells and was activated in replicatively and prematurely senescent TIG-1 cells. The causative role of PKC-{delta} in cellular senescence programs was demonstrated using a kinase negative PKC-{delta} and small interfering RNA against PKC-{delta}. Furthermore, PKC-{delta} was shown to function in human telomerase reverse transcriptase (hTERT) gene repression. These results indicate that PKC-{delta} plays a key role in cellular senescence programs, and suggest that the induction of senescence and hTERT repression are coordinately regulated by PKC-{delta}.

Key Words: hTERT, PKC-{delta}, senescence, TGF-β, TIG-1

Abbreviations: BrdU, bromodeoxyuridine; FBS, fetal bovine serum; hTERT, human telomerase reverse transcriptase; PKC-{delta} KN, kinase-negative type PKC-{delta}; moi, multiplicity of infection; PKC-{delta} CF, PKC-{delta} catalytic fragment; PDL, population doubling level; PKC, protein kinase C; SA-β-Gal, senescence-associated β-galactosidase; siRNA, small interfering RNA; TAK1, TGF-β-activated kinase 1; TGF-β, transforming growth factor β

{dagger}These authors contributed equally to this work.


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