Effect of Babao Dan on angiogenesis of gastric cancer in vitro by regulating VEGFA/VEGFR2 signaling pathway

被引:10
|
作者
Guan, Jian-Hua [1 ]
Cao, Zhi-Yun [1 ,2 ]
Guan, Bin [3 ]
Wei, Li-Hui [1 ,2 ]
Peng, Jun [1 ,2 ]
Chen, You-Qin [1 ,4 ]
Sferra, Thomas Joseph [1 ,4 ]
Sankararaman, Senthilkumar [1 ,4 ]
Zhan, Zhi-Xue [3 ]
Lin, Jiu-Mao [1 ,2 ]
机构
[1] Fujian Univ Tradit Chinese Med, Acad Integrat Med, 1 Qiuyang Rd, Fuzhou 350122, Fujian, Peoples R China
[2] Fujian Univ Tradit Chinese Med, Fujian Key Lab Integrat Med Geriatr, Fuzhou, Peoples R China
[3] Xiamen Tradit Chinese Med Co Ltd, Xiamen, Peoples R China
[4] Case Western Reserve Univ, Rainbow Babies & Childrens Hosp, Sch Med, Dept Pediat, Cleveland, OH 44106 USA
关键词
Babao Dan (BBD); gastric cancer (GC); angiogenesis; human umbilical vein endothelial cells (HUVECs); vascular endothelial growth factor A (VEGFA); vascular endothelial growth factor receptor 2 (VEGFR2); TUMOR ANGIOGENESIS; VEGF; GROWTH; METASTASIS; EXPRESSION; FORMULA; VIVO;
D O I
10.21037/tcr-20-2559
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: To further elucidate the anti-angiogenesis effect of Babao Dan (BBD) in vitro, gastric cancer (GC) cells and human umbilical vein endothelial cells (HUVECs) were used to evaluate the regulation role of BBD by vascular endothelial growth factor A (VEGFA)/vascular endothelial growth factor receptor 2 (VEGFR2) signaling pathway. Methods: After induced by VEGFA, GC cells (AGS, MGC80-3 and BGC823) were treated by different concentrations of BBD and then were detected cell viability, migration and VEGFA level. And the anti-angiogenesis effect of BBD was evaluated with HUVECs. To furtherly mimic the tumor microenvironment of angiogenesis, VEGFA as an inducer (10 ng/mL) was used to trigger a cascade of angiogenesis of HUVECs in vitro. Results: The viability and migration of GC cells with VEGFA-induced or non-induced and VEGFA levels in GC cells were significantly inhibited by BBD with concentration-dependent manner (P<0.01). BBD significantly inhibited the HUVECs viability with concentration-dependent manner (P<0.01), which was consistent with the inhibitory action on augmentation of cell viability induced by VEGFA ( P<0.01). BBD exhibited the similar inhibitory trend on cyto behavioral variability such as wound repairing (P<0.05), migration (P<0.01) and tube formation (P<0.01) and activation effect on cell apoptosis rate (P<0.01) with VEGFA-induced or non-induced. Moreover, BBD notably regulated the levels of VEGFA, VEGFR2, matrix metalloprotein 2 (MMP2) and matrix metalloprotein 9 (MMP9) of HUVECs on present or absent of VEGFA with dose-dependent manner. Conclusions: BBD inhibited GC growth against VEGFA-induced angiogenesis of HUVECs by VEGFA/VEGFR2 signaling pathway in vitro.
引用
收藏
页码:953 / +
页数:15
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