Jin Fu Kang Oral Liquid Inhibits Lymphatic Endothelial Cells Formation and Migration

被引:8
作者
He, Hai-Lang [1 ]
Wang, Dan [1 ]
Tang, Jie [1 ]
Zhou, Xian-Mei [1 ]
Li, Jian-Xin [2 ,3 ]
Xu, Ling [4 ,5 ]
机构
[1] Nanjing Univ Chinese Med, Affiliated Jiangsu Prov Hosp Tradit Chinese Med, Dept Resp Med, Nanjing 210029, Jiangsu, Peoples R China
[2] Nanjing Univ, Sch Chem & Chem Engn, State Key Lab Analyt Chem Life Sci, Nanjing 210023, Jiangsu, Peoples R China
[3] Nanjing Univ, Sch Chem & Chem Engn, Collaborat Innovat Ctr Chem Life Sci, Nanjing 210023, Jiangsu, Peoples R China
[4] Shanghai Univ Tradit Chinese Med, Tumor Inst Tradit Chinese Med, 725 South Wanping Rd, Shanghai 200032, Peoples R China
[5] Shanghai Univ Tradit Chinese Med, Yueyang Hosp Integrated Tradit Chinese & Western, Dept Oncol, 110 Ganhe Rd, Shanghai 200437, Peoples R China
关键词
PROGENITOR CELLS; CANCER; LYMPHANGIOGENESIS; ANGIOGENESIS; METASTASIS; MECHANISMS; GROWTH; CXCR4;
D O I
10.1155/2016/3635209
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Lung cancer is the leading cause of cancer-related deaths worldwide. Jin Fu Kang (JFK), an oral liquid prescription of Chinese herbal drugs, has been clinically available for the treatment of non-small cell lung cancer (NSCLC). Lymphangiogenesis is a primary event in the process of cancer development and metastasis, and the formation and migration of lymphatic endothelial cells (LECs) play a key role in the lymphangiogenesis. To assess the activity of stromal cell-derived factor-1 (SDF-1) and the coeffect of SDF-1 and vascular endothelial growth factor-C (VEGF-C) on the formation and migration of LECs and clarify the inhibitory effects of JFK on the LECs, the LECs were differentiated from CD34(+)/VEGFR-3(+) endothelial progenitor cells (EPCs), and JFK-containing serums were prepared from rats. SDF-1 and VEGF-C both induced the differentiation of CD34(+)/VEGFR-3(+) EPCs towards LECs and enhanced the LECs migration. Couse of SDF-1 and VEGF-C displayed an additive effect on the LECs formation but not on their migration. JFK inhibited the formation and migration of LECs, and the inhibitory effects were most probably via regulation of the SDF-1/CXCR4 and VEGF-C/VEGFR-3 axes. The current finding suggested that JFK might inhibit NSCLC through antilymphangiogenesis and also provided a potential to discover antilymphangiogenesis agents from natural resources.
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页数:10
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