@Article{096504021X16137463165424,
AUTHOR = {Juan Gu, Chang-fu Cui, Li Yang, Ling Wang, Xue-hua Jiang},
TITLE = {Emodin Inhibits Colon Cancer Cell Invasion and Migration by Suppressing  Epithelial–Mesenchymal Transition via the Wnt/β-Catenin Pathway},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {6},
PAGES = {681--682},
URL = {http://www.techscience.com/or/v28n6/48504},
ISSN = {1555-3906},
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.},
DOI = {10.3727/096504021X16137463165424}
}