Abstract
Arctigenin (ARC) has been shown to have an anti-cancer effect in various cell types and tissues. However, there have been no studies concerning metastatic colorectal cancer (CRC). In this study, we investigated the anti-metastatic properties of ARC on colorectal metastasis and present a potential candidate drug. ARC induced cell cycle arrest and apoptosis in CT26 cells through the intrinsic apoptotic pathway via MAPKs signaling. In several metastatic phenotypes, ARC controlled epithelial-mesenchymal transition (EMT) through increasing the expression of epithelial marker E-cadherin and decreasing the expressions of mesenchymal markers; N-cadherin, vimentin, β-catenin, and Snail. Moreover, ARC inhibited migration and invasion through reducing of matrix metalloproteinase-2 (MMP-2) and MMP-9 expressions. In an experimental metastasis model, ARC significantly inhibited lung metastasis of CT26 cells. Taken together, our study demonstrates the inhibitory effects of ARC on colorectal metastasis.
Highlights
Arctigenin (ARC), a lignan-derived compound, is isolated from various kinds of plants such as Arctium lappa Linné (Arctii Fructus) and Forsythia suspensa Vahl (Forsythia Fruit) [1,2]
We investigate the anti-metastatic effects of ARC using metastatic colon cancer cell lines and an experimental animal metastasis model
Expression of cyclin cyclin E, and cyclin-dependent kinase subunits (CDKs) 2 (Figure 2c). These results indicate that ARC-mediated cell cycle arrest in CT26 cyclin
Summary
Arctigenin (ARC), a lignan-derived compound, is isolated from various kinds of plants such as Arctium lappa Linné (Arctii Fructus) and Forsythia suspensa Vahl (Forsythia Fruit) [1,2]. Molecules 2016, 21, 1135 oxide and inducible nitric oxide synthase as well as p38 mitogen-activated protein kinase (MAPK) and nuclear transcription factor-kappa B (NF-κB) pathways, which contribute to cancer cell growth and survival [4,5]. It remains unclear whether ARC has inhibitory effects on colorectal metastasis. MMPs are extracellular proteases and zinc-binding endopeptidases which are related to the degradation of extracellular matrix (ECM) and affect a crucial role in metastasis such as cancer cell growth, migration and invasion. We investigate the anti-metastatic effects of ARC using metastatic colon cancer cell lines and an experimental animal metastasis model
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