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Journal of Biochemistry Advance Access published online on March 11, 2009
Journal of Biochemistry, 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 Katakura1,2,3,4,5, Miyako Udono2,4, 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

5Correspondence should be addressed to Dr. Yoshinori Katakura. Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan. E-mail: katakura@grt.kyushu-u.ac.jp, Tel & Fax: +81-92-642-3050

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}. Further, 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 coordinatedly regulated by PKC-{delta}.

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

4The first two authors contributed equally to this work.


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