Poly I:C inhibits cell proliferation and enhances the growth inhibitory effect of paclitaxel in oral sqaumous cell carcinoma

Authors

  • Jong-Hwan Park Department of Biochemistry, College of Medicine, Konyang University, Daejeon, Korea
  • Do-In Jeon Department of Pathology and Research Center for Oral Disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea
  • Hyo-Eun Yoon Department of Pathology and Research Center for Oral Disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea
  • Seong-Min Kwon Department of Pathology and Research Center for Oral Disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea
  • Soo-A Kim Department of Biochemistry, College of Oriental Medicine, Dongguk University, Gyungju, Korea
  • Sang-Gun Ahn Department of Pathology and Research Center for Oral Disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea
  • Jung-Hoon Yoon Department of Pathology and Research Center for Oral Disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea

DOI:

https://doi.org/10.3109/00016357.2011.640278

Keywords:

Toll-like receptor 3 (TLR3), Poly I:C, oral sqaumous cell carcinoma, apoptosis, paclitaxel

Abstract

Objective. Toll-like receptors (TLR) signaling has dual effect of promoting tumor progression and anti-cancer property. This study was designed to determine the effect of polyinosinic-polycytidilic acid (poly I:C), a TLR3 agonist, on the proliferation of oral cancer cells. Materials and methods: Human oral squamous cell carcinoma cell lines, YD-10B and YD-8, were used. TLRs expression was examined by RT-PCR and IL-8 production by poly I:C was examined by ELISA. Cell proliferation was determined by MTT assay. Flow cytometry and Western blot analysis were performed to determine the molecular mechanism of poly I:C-induced cell death. Results. TLR3 was functionally expressed in YD-10B and YD-8 cells. Treatment of poly I:C inhibited the cell growth in a dose-dependent manner. Flow cytometry and Western blot analysis revealed that poly I:C induced apoptosis via a mitochondria-dependent pathway. In addition, combination treatment with poly I:C and paclitaxel more significantly inhibited cell proliferation compared with poly I:C or paclitaxel alone. Conclusions. Poly I:C effectively inhibits oral cancer cell proliferation and can be considered as a candidate to improve the inhibitory effect of anti-cancer drugs.

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Published

2012-05-01