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Parthenolide promotes apoptotic cell death and inhibits the migration and invasion of SW620 cells
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Yu Chuan Liu, Se Lim Kim, Young Ran Park, Soo-Teik Lee, Sang Wook Kim
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Intest Res 2017;15(2):174-181. Published online April 27, 2017
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DOI: https://doi.org/10.5217/ir.2017.15.2.174
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Abstract
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- Background/Aims
Parthenolide (PT), a principle component derived from feverfew (Tanacetum parthenium), is a promising anticancer agent and has been shown to promote apoptotic cell death in various cancer cells. In this study, we focused on its functional role in apoptosis, migration, and invasion of human colorectal cancer (CRC) cells. MethodsSW620 cells were employed as representative human CRC cells. We performed the MTT assay and cell cycle analysis to measure apoptotic cell death. The wound healing, Transwell migration, and Matrigel invasion assays were performed to investigate the effect of PT on cell migration/invasion. Western blotting was used to establish the signaling pathway of apoptosis and cell migration/invasion. ResultsPT exerts antiproliferative effect and induces apoptotic cell death of SW620 cells. In addition, PT prevents cell migration and invasion in a dose-dependent manner. Moreover, PT markedly suppressed migration/invasion-related protein expression, including E-cadherin, β-catenin, vimentin, Snail, cyclooxygenase-2, matrix metalloproteinase-2 (MMP-2), and MMP-9 in SW620 cells. PT also inhibited the expression of antiapoptotic proteins (Bcl-2 and Bcl-xL) and activated apoptosis terminal factor (caspase-3) in a dose-dependent manner. ConclusionsOur results suggest that PT is a potential novel therapeutic agent for aggressive CRC treatment.
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Citations
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