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Korean Society for Biochemistry and Molecular Biology (생화학분자생물학회)
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TC1 (C8orf4) is involved in ERK1/2 pathway-regulated G1- to S-phase transition

  • Wang, Yi-Dong (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Bian, Guo-Hui (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Lv, Xiao-Yan (Department of Dermatology, West China Hospital, Sichuan University) ;
  • Zheng, Rong (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Sun, Huan (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Zhang, Zheng (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Chen, Ye (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Li, Qin-Wei (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Xiao, Yan (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Yang, Qiu-Tan (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Ai, Jian-Zhong (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Wei, Yu-Quan (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University) ;
  • Zhou, Qin (Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University)
  • Published : 2008.10.31
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Abstract

Although previous studies have implicated a role for TC1 (C8orf4) in cancer cell proliferation, the molecular mechanism of its action is still largely unclear. In this study, we showed, for the first time, that the mRNA levels of TC1 were upregulated by mitogens (FBS/thrombin) and at least partially, through the ERK1/2 signaling pathway. Interestingly, the over-expression of TC1 promoted the $G_1$- to S-phase transition of the cell cycle, which was delayed by the deficiency of ERK1/2 signaling in fibroblast cells. Furthermore, the luciferase reporter assay indicated that the over-expression of TC1 significantly increased Cyclin D1 promoter-driven luciferase activity. Taken together, our findings revealed that TC1 was involved in the mitogen-activated ERK1/2 signaling pathway and positively regulated $G_1$- to S-phase transition of the cell cycle. Our results may provide a novel mechanism of the role of TC1 in the regulation of cell proliferation.

Keywords

References

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