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Interference of Fisetin with Targets of the Nuclear Factor-κB Signal Transduction Pathway Activated by Epstein-Barr Virus Encoded Latent Membrane Protein 1

  • Li, Rong (Department of Pathology and Pathophysiology, School of Basic Medicine Science) ;
  • Liang, Hong-Ying (Laboratory of Physiological Science, Guangdong Medical College) ;
  • Li, Ming-Yong (Department of Pathology and Pathophysiology, School of Basic Medicine Science) ;
  • Lin, Chun-Yan (Laboratory of Physiological Science, Guangdong Medical College) ;
  • Shi, Meng-Jie (Department of Pathology and Pathophysiology, School of Basic Medicine Science) ;
  • Zhang, Xiu-Juan (Department of Physiology, School of Basic Medicine Science)
  • Published : 2014.12.18

Abstract

Fisetin is an effective compound extracted from lacquer which has been used in the treatment of various diseases. Preliminary data indicate that it also exerts specific anti-cancer effects. However, the manner in which fisetin regulates cancer growth remains unknown. In this study, we elucidated interference of fisetin with targets of the nuclear factor ${\kappa}B$ signal transduction pathway activated by Epstein-Barr virus encoding latent membrane protein 1 (LMP1)in nasopharyngeal carcinoma (NPC) cells, Results showed that fisetin inhibited the survival rate of CNE-LMP1 cells and NF-${\kappa}B$ activation caused by LMP1. Fisetin also suppressed nuclear translocation of NF-${\kappa}B$ (p65) and $I{\kappa}B{\alpha}$ phosphorylation, while inhibiting CyclinD1, all key targets of the NF-${\kappa}B$ signal transduction pathway. It was suggested that interference effects of fisetin with signal transduction activated by LMP1 encoded by the Epstein-Barr virus may play an important role in its anticancer potential.

Keywords

References

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