期刊
JOURNAL OF NEURO-ONCOLOGY
卷 128, 期 2, 页码 217-223出版社
SPRINGER
DOI: 10.1007/s11060-016-2107-z
关键词
Phloretin; Cell cycle arrest; Apoptosis; Reactive oxygen species; Glioblastoma
资金
- National S&T Major Project of China [2012ZX09303-005-003]
- 973 National ST Major Project [2011CB503900]
- National Natural Science Foundation of China [81370235, 81170101]
- Natural Science Foundation of Beijing [7122106]
Phloretin, a flavonoid present in various plants, has been reported to exert anticarcinogenic effects. However, the mechanism of its chemo-preventive effect on human glioblastoma cells is not fully understood. This study aimed to investigate the molecular mechanism of phloretin and its associated chemo-preventive effect in human glioblastoma cells. The results indicate that phloretin inhibited cell proliferation by inducing cell cycle arrest at the G0-G1 phase and induced apoptosis of human glioblastoma cells. Phloretin-induced cell cycle arrest was associated with increased expression of p27 and decreased expression of cdk2, cdk4, cdk6, cyclinD and cyclinE. Moreover, the PI3K/AKT/mTOR signaling cascades were suppressed by phloretin in a dose-dependent manner. In addition, phloretin triggered the mitochondrial apoptosis pathway and generated reactive oxygen species (ROS). This was accompanied by the up-regulation of Bax, Bak and c-PARP and the down-regulation of Bcl-2. The antioxidant agents N-acetyl-l-cysteine and glutathione weakened the effect of phloretin on glioblastoma cells. In conclusion, these results demonstrate that phloretin exerts potent chemo-preventive activity in human glioblastoma cells through the generation of ROS.
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