Abstract B74: EGCG inhibits cancer invasion by regulating tumor-stromal crosstalk in oral squamous cell carcinoma

Abstract

Abstract Introduction: Epigallocatechin-3-O-gallate (EGCG), a major constituent polyphenol of green tea, has been shown to have suppressive effects on the invasion of various cancer cells, whereas the exact mechanisms have not yet been fully elucidated. In this study, the effects of EGCG on the invasion of oral squamous cell carcinoma (OSCC) were investigated where the new perspective focused on tumor-stromal crosstalk was emphasized, unlikely other previous studies focused on cancer cell mainly. Materials and Methods: OSCC were cultured with or without carcinoma-associated fibroblasts (CAF) in the dose dependent treatment of EGCG. In order to investigate the invasiveness, invasion assay and zymography were examined. Based on our previous study found that several cytokines are concerned with tumor-stromal crosstalk in invasion of OSCC, RT-PCR and ELISA assay were employed to examine the influence of EGCG on the expression levels of cytokines. Results: The invasiveness of OSCC was reduced by EGCG treatment, and the 50% reduction was demonstrated at the half concentration of EGCG (25 μM) in co-cultured group with CAF, compared to OSCC mono-cultured (50 μM). Zymography showed that EGCG treatment reduced MMP-9 expression in co-cultured condition. In addition, EGCG resulted in a noticeable decrease in the expression of cytokines, especially GRO-α/CXCL1, concerned with tumor-stromal crosstalk in invasion of OSCC. Conclusions: In this study, inhibitory effect of EGCG on cancer invasion was found at which its concentration is lower than previously known. Taking these results into consideration, EGCG may play an effective role in preventing invasion of OSCC by regulating tumor-stromal crosstalk. Acknowledgement: This work was supported by Priority Research Centers Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010–0029702). Citation Information: Cancer Prev Res 2011;4(10 Suppl):B74.