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

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.

Key Words::

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

Acknowledgment

This study was supported by grants of the Korea Science and Engineering Foundation (KOSEF) funded by the Korea government (MOST) (Grant No. R13-2008-010-00000-0).

Declaration of interest : The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.