Intest Res  
Parthenolide promotes apoptotic cell death and inhibits the migration and invasion of SW620 cells
Yu Chuan Liu1,2*, Se Lim Kim1,2*, Young Ran Park1,2, Soo-Teik Lee1,2, Sang Wook Kim1,2
1Department of Internal Medicine, Research Institute of Clinical Medicine of Chonbuk National University Hospital, 2Biomedical Research Institute of Chonbuk National University Hospital, Chonbuk National University Medical School, Jeonju, Korea
Correspondence to: Sang Wook Kim, Department of Internal Medicine, Research Institute of Clinical Medicine of Chonbuk National University Hospital, 20 Geonji-ro, Deokjin-gu, Jeonju 54907, Korea. Tel: +82-63-250- 2302, Fax: +82-63-254-1609, E-mail:
*These authors contributed equally to this study.
Received: April 8, 2016; Revised: June 14, 2016; Accepted: June 14, 2016; Published online: March 21, 2017.
© Korean Association for the Study of Intestinal Diseases. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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 onits functional role in apoptosis, migration, and invasion of human colorectal cancer (CRC) cells. Methods: SW620 cells wereemployed as representative human CRC cells. We performed the MTT assay and cell cycle analysis to measure apoptotic celldeath. The wound healing, Transwell migration, and Matrigel invasion assays were performed to investigate the effect of PT oncell migration/invasion. Western blotting was used to establish the signaling pathway of apoptosis and cell migration/invasion.Results: PT 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 inSW620 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. Conclusions: Our results suggest that PT is a potential novel therapeutic agentfor aggressive CRC treatment.
Keywords: Colorectal neoplasms; Parthenolide; Apoptosis; Migration; Invasion

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