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学科主题临床医学
Suppression of renal cell carcinoma growth in vivo by forced expression of vascular endothelial growth inhibitor
Zhang, Ning1; Wu, Pengjie3; Shayiremu, Duoerkun5; Wu, Liyang1; Shan, Hui1; Ye, Lin2; Zhao, Xueqin4; Cai, Jie4; Jiang, Wen Guo2; Gong, Kan3; Yang, Yong1
关键词vascular endothelial growth inhibitor renal cell carcinoma angiogenesis target therapy
刊名INTERNATIONAL JOURNAL OF ONCOLOGY
2013-05-01
DOI10.3892/ijo.2013.1877
42期:5页:1664-1673
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
研究领域[WOS]Oncology
关键词[WOS]TNF-LIKE LIGAND ; TUMOR-GROWTH ; ANGIOGENESIS INHIBITOR ; UNITED-STATES ; KIDNEY CANCER ; T-CELL ; TL1A ; CYTOKINE ; VEGI ; THERAPY
英文摘要

Vascular endothelial growth inhibitor (VEGI) has been associated with tumor-related vasculature in certain malignancies. However, its implication in renal cell carcinoma (RCC), an angiogenesis-dependent tumor, remains unknown. In the present study, we investigated the role played by VEGI in RCC. The expression of VEGI was examined in human renal tissue and RCC cell lines using immunohistochemical staining and RT-PCR, respectively. The biological impact of modifying the expression of VEGI in RCC cells was evaluated using in vitro and in vivo models. We show that VEGI mRNA is expressed in a wide variety of human RCC cell lines, all of normal renal and most of RCC tissue specimens. VEGI protein expression was observed in normal renal tubular epithelial cells, but was decreased or absent in RCC specimens, particularly in tumors with high grade. Moreover, forced expression of VEGI led to an inhibition of vascular endothelial tube formation, decrease in the motility and adhesion of RCC cells in vitro. Interestingly, forced expression of VEGI had no bearing on growth, apoptosis and invasive capacity of RCC cells. However, tumor growth was reduced in xenograft models. Immunohistochemical staining showed that microvessel density decreased in VEGI forced expression xenograft tumor samples. Taken together, our findings showed that the expression of VEGI is decreased in RCC, particularly in tumors with higher grade. Together with its inhibitory effect on cellular motility, adhesion, vascular endothelial tube formation and tumor growth in vivo, this suggests that VEGI functions mainly through inhibition of angiogenesis and is a negative regulator of aggressiveness during the development and progression of RCC.

语种英语
WOS记录号WOS:000318053400019
项目编号81072088
资助机构National Natural Science Foundation of China ; Cancer Research Wales
引用统计
被引频次:3[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/65318
专题北京大学第一临床医学院_泌尿外科
作者单位1.Capital Med Univ, Beijing Chaoyang Hosp, Dept Urol, Beijing 100020, Peoples R China
2.Cardiff Univ, Sch Med, Metastasis & Angiogenesis Res Grp, Cardiff CF14 4XN, S Glam, Wales
3.Peking Univ, Hosp 1, Dept Urol, Beijing 100034, Peoples R China
4.Crown Biosci Inc, Div Translat Oncol, Santa Clara, CA 95054 USA
5.Cent Hosp HaMi Reg XinJiang Prov, Dept Urol, XinJiang, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Ning,Wu, Pengjie,Shayiremu, Duoerkun,et al. Suppression of renal cell carcinoma growth in vivo by forced expression of vascular endothelial growth inhibitor[J]. INTERNATIONAL JOURNAL OF ONCOLOGY,2013,42(5):1664-1673.
APA Zhang, Ning.,Wu, Pengjie.,Shayiremu, Duoerkun.,Wu, Liyang.,Shan, Hui.,...&Yang, Yong.(2013).Suppression of renal cell carcinoma growth in vivo by forced expression of vascular endothelial growth inhibitor.INTERNATIONAL JOURNAL OF ONCOLOGY,42(5),1664-1673.
MLA Zhang, Ning,et al."Suppression of renal cell carcinoma growth in vivo by forced expression of vascular endothelial growth inhibitor".INTERNATIONAL JOURNAL OF ONCOLOGY 42.5(2013):1664-1673.
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