Thida, Mya Kim, Dae Won Thi Thu Thuy Tran Minh Quan Pham Lee, Heesu Kim, Inki Lee, Jae Wook 2024-01-20T05:01:38Z 2024-01-20T05:01:38Z 2021-09-05 2016-02-01 0960-894X https://pubs.kist.re.kr/handle/201004/124411 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. (C) 2015 Elsevier Ltd. All rights reserved. English Pergamon Press Ltd. CYCLE ARREST INHIBITION PHOSPHORYLATION TEMOZOLOMIDE TARGET Gambogic acid induces apoptotic cell death in T98G glioma cells Article 10.1016/j.bmcl.2015.11.043 1 Bioorganic & Medicinal Chemistry Letters, v.26, no.3, pp.1097 - 1101 Bioorganic & Medicinal Chemistry Letters 26 3 1097 1101 scie scopus 000368797600079 2-s2.0-84979197943 Chemistry, Medicinal Chemistry, Organic Pharmacology & Pharmacy Chemistry Article CYCLE ARREST INHIBITION PHOSPHORYLATION TEMOZOLOMIDE TARGET Gambogic acid Reactive oxygen species (ROS) Glioblastoma Apoptosis Anticancer