Tectorigenin Inhibits Glioblastoma Proliferation by G0/G1 Cell Cycle Arrest

被引:14
作者
Yeh, Liang-Tsai [1 ]
Hsu, Li-Sung [2 ,3 ]
Chung, Yi-Hsuan [4 ]
Chen, Chih-Jung [5 ,6 ]
机构
[1] Changhua Christian Hosp, Dept Anesthesiol, Changhua 500, Taiwan
[2] Chung Shan Med Univ, Inst Med, Taichung 402, Taiwan
[3] Chung Shan Med Univ Hosp, Clin Lab, Taichung 402, Taiwan
[4] Chung Shan Med Univ, Inst Biochem Microbiol & Immunol, Taichung 402, Taiwan
[5] Chung Shan Med Univ, Sch Med, Taichung 402, Taiwan
[6] Taichung Vet Gen Hosp, Dept Pathol & Lab Med, Taichung 407, Taiwan
来源
MEDICINA-LITHUANIA | 2020年 / 56卷 / 12期
关键词
glioblastoma; tectorigenin; molecular mechanism; in vitro model; cell cycle arrest; DEPENDENT KINASES; DOWN-REGULATION; CANCER CELLS; APOPTOSIS; AKT; ACTIVATION; TARGETS; MAPK;
D O I
10.3390/medicina56120681
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background and objectives: Glioblastoma is one of the leading cancer-related causes of death of the brain region and has an average 5-year survival rate of less than 5%. The aim of this study was to investigate the effectiveness of tectorigenin, a naturally occurring flavonoid compound with anti-inflammatory, anti-oxidant, and anti-tumor properties, as a treatment for glioblastoma. A further goal was to use in vitro models to determine the underlying molecular mechanisms. Materials and Methods: Exposure to tectorigenin for 24 h dose-dependently reduced the viability of glioblastoma cells. Results: Significant cell cycle arrest at G0/G1 phase occurred in the presence of 200 and 300 mu M tectorigenin. Treatment with tectorigenin clearly reduced the levels of phosphorylated retinoblastoma protein (p-RB) and decreased the expression of cyclin-dependent protein 4 (CDK4). Tectorigenin treatment also significantly enhanced the expression of p21, a CDK4 inhibitor. Conclusions: Collectively, our findings indicated that tectorigenin inhibited the proliferation of glioblastoma cells by cell cycle arrest at the G0/G1 phase.
引用
收藏
页码:1 / 9
页数:9
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