Gambogic acid induces cell apoptosis through endoplasmic reticulum stress triggered inhibition of Akt signaling pathways in extranodal NK/T-cell lymphoma cells.
10.1016/S1875-5364(18)30109-2
- Author:
Wei PENG
1
;
Bao-An CHEN
2
Author Information
1. Department of Medical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing 210009, China. Electronic address: wpeng01@hotmail.com.
2. Department of Hematology and Oncology (Key Department of Jiangsu Medicine), Medical School, the Affiliated Zhongda Hospital, Southeast University, Nanjing 210009, China. Electronic address: baoan_chen@yeah.net.
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Endoplasmic reticulum stress;
Extranodal NK/T-cell lymphoma;
Gambogic acid
- MeSH:
Apoptosis;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Endoplasmic Reticulum Stress;
drug effects;
Humans;
Lymphoma, Extranodal NK-T-Cell;
drug therapy;
genetics;
metabolism;
physiopathology;
Proto-Oncogene Proteins c-akt;
genetics;
metabolism;
Signal Transduction;
drug effects;
Xanthones;
pharmacology
- From:
Chinese Journal of Natural Medicines (English Ed.)
2018;16(9):693-699
- CountryChina
- Language:English
-
Abstract:
As the chemotherapeutic resistance of extranodal NK/T-cell lymphoma (ENKTL) rises year by year, searching for novel chemoprevention compounds has become imminent. Gambogic acid (GA) has recently been shown to have anti-tumor effects, but its role and underling mechanism in ENKTL are rather elusive. In the present study, we showed that GA inhibited the cell growth and potently induced the apoptosis of ENKTL cells in vitro in a time- and concentration-dependent manner. Furthermore, GA induced cell death through endoplasmic reticulum stress (ERS) mediated suppression of Akt signaling pathways and finally the release of the caspase-3 proteases. Overall, our data provided evidences supporting GA as a potential therapeutic agent for ENKTL, which may facilitate further preclinical development of anti-tumor drugs.
