The Signaling Mechanism Underlying the Growth Inhibitory Effect of Resveratrol in Human Colorectal Carcinoma Cell Lines

• Main Authors: Lee-Chin Leh ( Julie Leh ), 呂麗琴
• Other Authors: Shiu-Feng Tung
• Format: Others
• Language: zh-TW
• Published: 2003
• Online Access: http://ndltd.ncl.edu.tw/handle/25759949381653129753

碩士 === 實踐大學 === 食品營養研究所 === 91 === Resveratrol is a polyphenolic compound that act as a phytoalexin in plant. Recent studies showed that resveratrol might exert anti-oxidative, anti-inflammatory and anti-carcinogenetic activity in animal cells. b-catenin is a cellular protein maintaining normal cell-cell adhesion function. Deregulated metabolic pathway of b-catenin might result in abnormal accumulation of b-catenin in cells, and induce the formation of b-catenin/TCF4 complex. Subsequently, b-catenin/TCF4 complex translocates into the nucleus to activate the transcription of several target genes. The downstream target genes of b-catenin/TCF4, such as c-myc and cycD1, are usually related to cell growth. It has been shown that Myc and Cyclin D1 might play an important role in the progression of human colon cancer. Recent studies indicate that resveratrol could, partly via inhibition of the activity of enzymes related to the production of pro-inflammatory precursors, decrease the oncogenecity of cancer cells. Our study is aimed to elucidate the potential mechanism underlying the growth inhibitory activity of resveratrol in colorectal carcinoma cells. First, MTT ( 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide ) assay was used to evaluate the growth inhibitory activity of resveratrol in colorectal carcinoma cells. Second, reporter plasmids were transfected into those cell lines to analyze the effect of resveratrol on transcriptional activation mediated by b-catenin/TCF4 complex. Finally, we used Western blotting to investigate the protein expression pattern affected by resveratrol in colorecatal carcinoma cells. We propose that resveratrol could decrease colon cancer cell’s growth ability via downregulation of b-catenin expression in wild-type p53-deficient colon cancer cells.