| Summary: | 碩士 === 實踐大學 === 食品營養研究所 === 91 === Abstract
Apigenin is a plant flavonoid that is thought to play a role in the prevention of carcinogenesis. The molecular mechanism underlying the action of apigenin has not been elucidated yet. The Wnt/Wingless signaling transduction pathway plays an important role in both embryonic development and tumorigenesis. β-catenin, a key component of the Wnt signaling pathway, interacts with the TCF/LEF family of transcription factors and activates transcription of Wnt target genes. To evaluate the effect of apigenin on Wnt signaling pathway, we analyzed β-catenin-TCF4-mediated expression in colorectal carcinoma cells. Human colorectal HCT116 (wild-type p53), SW480 (mutant p53) and HT29 (mutant p53) cells were treated with various concentration of apigenin MTT assay demonostrated that treatment of above-mentioned colorectal carcinoma cells with apigenin (0-200 μM) resulted in a dose-dependent inhibition of growth of colorectal carcinoma cells. Werstern blot analysis of β-catenin in apigenin-treated colorectal carcinoma cells indicated that β-catenin decreased in a dose-dependent manner upon treatment. However, the downregulation of β-catenin protein level is not affected by cellular p53 status. β-catenin decreased in both wild-type p53- and mutant p53-containing colorectal carcinoma cells upon apigenin treatment.
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