Gambogic acid induces apoptotic cell death in T98G glioma cells

Authors
Thida, MyaKim, Dae WonThi Thu Thuy TranMinh Quan PhamLee, HeesuKim, InkiLee, Jae Wook
Issue Date
2016-02-01
Publisher
Pergamon Press Ltd.
Citation
Bioorganic & Medicinal Chemistry Letters, v.26, no.3, pp.1097 - 1101
Abstract
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.
Keywords
CYCLE ARREST; INHIBITION; PHOSPHORYLATION; TEMOZOLOMIDE; TARGET; CYCLE ARREST; INHIBITION; PHOSPHORYLATION; TEMOZOLOMIDE; TARGET; Gambogic acid; Reactive oxygen species (ROS); Glioblastoma; Apoptosis; Anticancer
ISSN
0960-894X
URI
https://pubs.kist.re.kr/handle/201004/124411
DOI
10.1016/j.bmcl.2015.11.043
Appears in Collections:
KIST Article > 2016
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