Colon cancer (CC) is the third most common cancer worldwide. Emodin is a kind of anthraquinone active substance which has the ability to affect tumor progression. Our study aims to explore the effects and the relevant mechanism of Emodin on the invasion and migration of CC in vitro and in vivo. In our study, we found that Emodin inhibited the invasion and migration ability of RKO cells and decreased the expression of Matrix metalloproteinase-7 (MMP-7), Matrix metalloproteinase-9 (MMP-9), and Vascular endothelial growth factor (VEGF) in a dose dependent manner. Further researches suggested that Emodin inhibited EMT by increasing the mRNA level of E-cadherin and decreasing the expression of N-cadherin, Snail and β-catenin. Emodin also significantly inhibited the activation of Wnt/β-catenin signaling pathway by down-regulating the expression of related downstream target genes, including TCF4, Cyclin-D1 and c-Myc. Besides, Wnt/β-catenin signaling pathway agonist obviously abolished the effect of Emodin on EMT and cell mobility, identifying that Emodin exerted its regulating role through the Wnt/β-catenin pathway. CC xenograft model was established to study the antitumor efficiency of Emodin in vivo. The in vivo study further demonstrated that Emodin (40mg/kg) suppressed tumor growth by inhibiting EMT via the Wnt/β-catenin signaling pathway in vivo. Taken together, we suggest that Emodin inhibits the invasion and migration of CC cells in vitro and in vivo by blocking EMT, which is related with the inhibition of Wnt/β-catenin signaling pathway.
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Department of Clinical Pharmacy, West China School of Pharmacy, Sichuan University, Sichuan 646000, China
Department of Neurology, Research Institute of China Weapons Industry, 521 Hospital, Shanxi 710000, China
Microbiological Laboratory, Xinyang Vocational and Technical College, Henan 464000, China
Appeared or available online: 04 January 2018