关键词: 萝卜硫素, 结肠癌, Wnt/β-catenin信号通路, 上皮间质转化

Abstract: In this study, HCT 116 colon cancer cells were used as a model to explore the effect of sulforaphane (SFN) on colon cancer cell proliferation, apoptosis, invasion and metastasis and further to uncover the potential mechanism of SFN on colon cancer cell invasion and metastasis. The results showed that SFN significantly inhibited the proliferation, invasion and metastasis of HCT 116 cells in a dose-dependent manner, and induced apoptosis. Furthermore, SFN inhibited the epithelial-mesenchymal transition (EMT) of HCT 116 cells by up-regulating the relative expression of the epithelial marker E-cadherin and down-regulating the expression of the mesenchymal markers N-cadherin, the snail family of transcriptional repressors (Snail), vimentin and matrix metalloproteinase 9. In addition, SFN significantly reduced the expression levels of β-catenin protein and its downstream effector molecules cyclin D1 and c-myc, and effectively blocked the activation of the Wnt/β-catenin signal pathway. SFN was able to effectively control the invasion and metastasis of colon cancer cells, and the mechanism may be related to the inhibition of the Wnt/β-catenin signaling pathway and EMT. This finding provides a new perspective to better understand the anti-cancer mechanism of SFN and offers a potential strategy for the dietary treatment of colon cancer.

Key words: sulforaphane, colon cancer, Wnt/β-catenin signaling pathway, epithelial-mesenchymal transition