Clock gene mouse period2 overexpression inhibits growth of human pancreatic cancer cells and has synergistic effect with cisplatin

O. D.A. Akira, Y. U. Katayose, Shinichi Yabuuchi, Kuniharu Yamamoto, Masamichi Mizuma, Satoru Shirasou, Toru Onogawa, Hideo Ohtsuka, Hiroshi Yoshida, Hiroki Hayashi, Toshiki Rikiyama, K. I.M. Hyunjung, Youngshik Choe, K. I.M. Kyungjin, S. O.N. Hosun, Fuyuhiko Motoi, Shinichi Egawa, Michiaki Unno

Research output: Contribution to journalArticlepeer-review

49 Citations (Scopus)

Abstract

Circadian rhythms are the daily oscillations of multiple biological processes regulated by an endogenous clock. The Period! gene is essential in controlling the circadian rhythm and plays an important role in tumor suppression. We examined whether the overexpression of the mouse Period! gene (mPer2) in cultured tumor cells from human tissues inhibits cell growth, using the recombinant adenovirus vector AdmPer2. The overexpression of mPer2 in human pancreatic cancer cells (Panel, Aspcl) reduced cellular proliferation and induced apoptotic cell death. Infection with AdmPer2 also inhibited cell-cycle progression, inducing arrest at the G 2-Mphase. Western blotting analyses confirmed that infection with AdmPer2 reduced Bcl-X L, Cdc2 and cyclin Bl protein, whereas it increased Box protein in Aspcl cells. The overexpression of mPer2 suppressed Cdc2 kinase activity. Moreover, infection with AdmPer2 resulted in.

Original languageEnglish
Pages (from-to)1201-1210
Number of pages10
JournalAnticancer research
Volume29
Issue number4
Publication statusPublished - 2009 Apr

Keywords

  • Apoptosis
  • Cell cycle arrest
  • Circadian rhythm
  • Cisplatin
  • Clock genes
  • Mouse period2 gene
  • Synergic effect
  • Tumor suppression

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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