Suppression of human pancreatic carcinoma cell growth and invasion by epigallocatechin-3-gallate.

INTRODUCTION: The consumption of green tea is associated with a lower risk of several types of human carcinomas. A number of studies have focused on the possible mechanisms of cancer prevention by tea extracts, especially polyphenols such as epigallocatechin-3-gallate (EGCG). AIMS AND METHODOLOGY: Green tea-derived EGCG was tested in human pancreatic carcinoma cells. The cells (PANC-1, MIA PaCa-2, and BxPC-3) were treated with different doses of EGCG (0, 25, 50, 100, and 200 micromol/L) for 48 hours in culture medium. Proliferation of pancreatic carcinoma cells was measured by means of the WST-1 colorimetric assay. For the study of cell invasion, the cells were incubated with 100 micromol/L EGCG for 2 hours. Then, the cells were added into the cell insert, coated with Matrigel basement membrane matrix. After incubation at 37 degrees C for 24 hours, the cells that had invaded through the Matrigel were counted visually under the microscope. RESULTS: The growth of all three pancreatic carcinoma cells was significantly suppressed by EGCG treatment in a dose-dependent manner. EGCG treatment caused significant suppression of the invasive ability of pancreatic carcinoma cells PANC-1, MIA PaCa-2, and BxPC-3 but did not affect the cell cycle protein cyclin D1. CONCLUSION: EGCG may be a potent biologic inhibitor of human pancreatic carcinomas, reducing their proliferative and invasive activities.

Suppressive effects of tea polyphenol and conformational changes with receptor for advanced glycation end products (RAGE) expression in human hepatoma cells.

BACKGROUND/AIMS: It is reported that polyphenol is associated with low risk of hepatoma and that RAGE (receptor for advanced glycation end products) is important for cancer invasion. METHODOLOGY: Effects of teapolyphenol, EGCG (epigallocatechin-3-gallate) were studied. Proliferation of on human hepatoma cells, HLF, was measured with the use of WST-1 colorimetric assay. Cell invasion was analyzed by the Matrigel invasion assay. Morphology and immunohistological staining of expression of RAGE were also performed. RESULTS: Proliferation was inhibited with the addition of EGCG in a dose-dependent manner. EGCG (200 mumol/L) produced a profound growth suppression of HLF cells (24.5%). Cell invasion was also inhibited with preincubation of 100 mumol/L of EGCG (10.2%). In addition to the antitumor effects, neurite-like conformational changes of HLF cells were observed. Addition of EGCG (100 mumol/L) showed the expression of RAGE on cell surface in accordance to the morphological changes. CONCLUSIONS: The pathway associated to cell movement might be activated with RAGE expression. Although EGCG inhibits the growth and invasion, the cells which expressed RAGE seem to survive. Thus, the enrollment of RAGE should be analyzed to clarify the mechanisms of cancer resistance.