Gambogic acid induces apoptotic cell death in T98G glioma cells
- Bioorg Med Chem Lett. 2016 Feb 1;26(3):1097-1101. doi: 10.1016/j.bmcl.2015.11.043.
- 1. Natural Product Research Center, Korea Institute of Science and Technology, Gangneung 210-340, Republic of Korea.
- 2. Department of Biochemistry and Molecular Biology, Research Institute of Oral Science, College of Dentistry, Gangneung Wonju National University, Gangneung 210-702, Republic of Korea.
- 3. Institute of Natural Products Research, Vietnamese Academy of Science and Technology, 18 Hoang Quoc Viet, Cay Giay, Hanoi, Viet Nam.
- 4. Department of Oral Anatomy, College of Dentistry, Gangneung Wonju National University, Gangneung 210-702, Republic of Korea.
- 5. Department of Medicine, University of Ulsan College of Medicine, Seoul 138-736, Republic of Korea; Asan Institute for Life Sciences, Asan Medical Center, Seoul 138-736, Republic of Korea. Electronic address: [email protected].
- 6. Natural Product Research Center, Korea Institute of Science and Technology, Gangneung 210-340, Republic of Korea; Department of Biological Chemistry, University of Science and Technology, Daejeun, Republic of Korea. Electronic address: [email protected].
Gambogic acid (GA), a natural product with a xanthone structure, has a broad range of anti-proliferative effects on Cancer cell lines. We evaluated GA for its cytotoxic effects on T98G glioblastoma cells. GA exhibited potent anti-proliferative activity and induced Apoptosis in T98G glioblastoma cells in a dose-dependent manner. Incubation of cells with GA revealed apoptotic features including increased Bax and AIF expression, cytochrome c release, and cleavage of Caspase-3, -8, -9, and PARP, while Bcl-2 expression was downregulated. Furthermore, GA induced Reactive Oxygen Species (ROS) generation in T98G cells. Our results indicate that GA increases Bax- and AIF-associated apoptotic signaling in glioblastoma cells.