Open Access

ARTICLE

Emodin Inhibits Colon Cancer Cell Invasion and Migration by Suppressing Epithelial–Mesenchymal Transition via the Wnt/β-Catenin Pathway

Juan Gu^*, Chang-fu Cui^†, Li Yang^‡, Ling Wang^*, Xue-hua Jiang^*

* Department of Clinical Pharmacy, West China School of Pharmacy, Sichuan University, Sichuan, P.R. China
† Department of Neurology, Research Institute of China Weapons Industry, 521 Hospital, Shanxi, P.R. China
‡ Microbiological Laboratory, Xinyang Vocational and Technical College, Henan, P.R. China

Oncology Research 2019, 27(2), 193-202. https://doi.org/10.3727/096504018X15150662230295

Retracted 17 July 2024

Abstract

Colon cancer (CC) is the third most common cancer worldwide. Emodin is an anthraquinone-active substance that 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 abilities of RKO cells and decreased the expression of matrix metalloproteinase-7 (MMP-7), MMP-9, and vascular endothelial growth factor (VEGF) in a dose-dependent manner. Further research 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 the Wnt/β-catenin signaling pathway by downregulating the expression of related downstream target genes, including TCF4, cyclin D1, and c-Myc. A Wnt/β-catenin signaling pathway agonist abolished the effect of emodin on EMT and cell mobility, suggesting that emodin exerted its regulating role through the Wnt/β-catenin pathway. The CC xenograft model was established to study the antitumor efficiency of emodin in vivo. The in vivo study further demonstrated that emodin (40 mg/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 the Wnt/β-catenin signaling pathway.

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