Decursin induces apoptosis in glioblastoma cells, but not in glial cells via a mitochondria-related caspase pathway
Seung Tack Oh1, Seongmi Lee2, Cai Hua3, Byung-Soo Koo4, Sok Cheon Pak5, Dong-Il-Kim6,*, Songhee Jeon3,*, Boo Ahn Shin7,*
1Research Institute, Dongkwang Pharmaceutical Company, Ltd., Seoul 04535, Korea, 2Department of Child and Adolescent Psychiatry, National Center for Mental Health, Seoul 04933, Korea, 3Department of Biomedical Sciences, Center for Creative Biomedical Scientists at Chonnam National University, Gwangju 61469, Korea, 4Department of Neuropsychiatry, College of Korean Medicine, Dongguk University, Goyang 10326, Korea, 5School of Biomedical Sciences, Charles Sturt University, Bathurst, NSW 2795 Australia, 6Department of Obstetrics & Gynecology, College of Korean Medicine, Dongguk University, Goyang 10326, Korea, 7Department of Microbiology and Immunology, Chonnam National University Medical School, Gwangju 61469, Korea
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Decursin is a major biological active component of Angelica gigas Nakai and is known to induce apoptosis of metastatic prostatic cancer cells. Recently, other reports have been commissioned to examine the anticancer activities of this plant. In this study, we evaluated the inhibitory activity and related mechanism of action of decursin against glioblastoma cell line. Decursin demonstrated cytotoxic effects on U87 and C6 glioma cells in a dose-dependent manner but not in primary glial cells. Additionally, decursin increased apoptotic bodies and phosphorylated JNK and p38 in U87 cells. Decursin also down-regulated Bcl-2 as well as cell cycle dependent proteins, CDK-4 and cyclin D1. Furthermore, decursin-induced apoptosis was dependent on the caspase activation in U87 cells. Taken together, our data provide the evidence that decursin induces apoptosis in glioblastoma cells, making it a potential candidate as a chemotherapeutic drug against brain tumor.