The inhibition mechanism and metabolic profile of phytochemicals in colorectal cancer cells

碩士 === 國立臺灣大學 === 食品科技研究所 === 100 ===   Colorectal cancer (CRC) is the third major cause of cancer-related mortality in Taiwan. The risk factors of CRC include age, family history, inflammatory bowel diseases, and environmental and dietary procarcinogens. In genetic phase, it goes through a series o...

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Bibliographic Details
Main Authors: Wan-Chi Tsai, 蔡婉琦
Other Authors: Been-Huang Chiang
Format: Others
Language:zh-TW
Published: 2012
Online Access:http://ndltd.ncl.edu.tw/handle/81320488291551679598
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Summary:碩士 === 國立臺灣大學 === 食品科技研究所 === 100 ===   Colorectal cancer (CRC) is the third major cause of cancer-related mortality in Taiwan. The risk factors of CRC include age, family history, inflammatory bowel diseases, and environmental and dietary procarcinogens. In genetic phase, it goes through a series of gene mutations, including APC, β-catenin and p53, from small benign precursor lesions to metastatic carcinomas. Based on information from literatures, this study chose six phytochemicals, including epigallocatechin gallate (EGCG), sulforaphane (SFN), phenethyl isothiocyanate (PEITC), 6-shogaol (SG), ursolic acid (UA) and resveratrol (RV), to investigate their effect on HT-29 and HCT 116 colorectal cancer cells in terms of regulating APC, β-catenin and p53. Then we selected the most effective one for further metabolic profile analysis. Results showed that resveratrol can suppress β-catenin, mutant p53 expression and increase wild-type p53 expression. And the metabolic profiling indicated that resveratrol can reduce taurine in both colorectal cancer cells, decrease hypoxanthine and 5’-methylthioadensine, enhance CMP in HT-29 cells. In HCT 116 cells, resveratrol is able to raise purine metabolism, TCA cycle and amino acid related metabolites. In conclusion, resveratrol may affect purine metabolism and TCA cycle by regulating wild-type p53 and mutant p53 expression.