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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 178178, 13 pages
Research Article

Activations of Both Extrinsic and Intrinsic Pathways in HCT 116 Human Colorectal Cancer Cells Contribute to Apoptosis through p53-Mediated ATM/Fas Signaling by Emilia sonchifolia Extract, a Folklore Medicinal Plant

1School of Pharmacy, China Medical University, Taichung 404, Taiwan
2Department of Life Sciences, National Chung Hsing University, Taichung 402, Taiwan
3Department of Biological Science and Technology, China Medical University, Taichung 404, Taiwan
4Department of Pharmacy, Da Chien General Hospital, Miaoli 360, Taiwan
5Department of Radiation Oncology, Chi Mei Medical Center, Tainan 710, Taiwan
6Department of Medical Education, Far Eastern Memorial Hospital, New Taipei 220, Taiwan
7Department of Biochemistry, Nihon Pharmaceutical University, Saitama 362-0806, Japan
8Tsuzuki Institute for Traditional Medicine, China Medical University, Taichung 404, Taiwan
9Department of Pharmacology, China Medical University, Taichung 40402, Taiwan

Received 17 August 2011; Revised 21 October 2011; Accepted 28 October 2011

Academic Editor: José Luis Ríos

Copyright © 2012 Yu-Hsuan Lan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Emilia sonchifolia (L.) DC (Compositae), an herbaceous plant found in Taiwan and India, is used as folk medicine. The clinical applications include inflammation, rheumatism, cough, cuts fever, dysentery, analgesic, and antibacteria. The activities of Emilia sonchifolia extract (ESE) on colorectal cancer cell death have not been fully investigated. The purpose of this study explored the induction of apoptosis and its molecular mechanisms in ESE-treated HCT 116 human colorectal cancer cells in vitro. The methanolic ESE was characterized, and γ-humulene was formed as the major constituent (63.86%). ESE induced cell growth inhibition in a concentration- and time-dependent response by MTT assay. Apoptotic cells (DNA fragmentation, an apoptotic catachrestic) were found after ESE treatment by TUNEL assay and DNA gel electrophoresis. Alternatively, ESE stimulated the activities of caspase-3, -8, and -9 and their specific caspase inhibitors protected against ESE-induced cytotoxicity. ESE promoted the mitochondria-dependent and death-receptor-associated protein levels. Also, ESE increased ROS production and upregulated the levels of ATM, p53, and Fas in HCT 116 cells. Strikingly, p53 siRNA reversed ESE-reduced viability involved in p53-mediated ATM/Fas signaling in HCT 116 cells. In summary, our result is the first report suggesting that ESE may be potentially efficacious in the treatment of colorectal cancer.