Parthenolide promotes apoptotic cell death and inhibits the migration and invasion of SW620 cells.
- Author:
Yu Chuan LIU
1
;
Se Lim KIM
;
Young Ran PARK
;
Soo Teik LEE
;
Sang Wook KIM
Author Information
- Publication Type:Original Article
- Keywords: Colorectal neoplasms; Parthenolide; Apoptosis; Migration; Invasion
- MeSH: Apoptosis; Blotting, Western; Cadherins; Cell Cycle; Cell Death*; Cell Movement; Colorectal Neoplasms; Cyclooxygenase 2; Humans; Matrix Metalloproteinase 2; Snails; Tanacetum parthenium; Vimentin; Wound Healing
- From:Intestinal Research 2017;15(2):174-181
- CountryRepublic of Korea
- Language:English
- Abstract: 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. METHODS: SW620 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. 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 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. CONCLUSIONS: Our results suggest that PT is a potential novel therapeutic agent for aggressive CRC treatment.
