中国癌症杂志 ›› 2014, Vol. 24 ›› Issue (12): 901-905.doi: 10.3969/j.issn.1007-3969.2014.12.004

• 论著 • 上一篇    下一篇

Vav3对人胃癌细胞株BGC823血管生成基因的调节作用及意义

檀碧波 李勇 范立侨 赵群 王冬 刘羽   

  1. 河北医科大学第四医院外三科,河北 石家庄 050011
  • 出版日期:2014-12-30 发布日期:2015-05-07
  • 通信作者: 李勇 E-mail:li_yong_hbth@126.com
  • 基金资助:
    国家自然科学基金资助项目(81072033、81372580);河北省自然科学基金资助项目(C2010000619);河北省普通高校强势特色学科资助项目(冀教高[2005]52);河北省科技支撑项目(14277779D);河北省卫生厅重大医学科研课题资助项目(zd2013040)。

Effect and significance of Vav3 to angiogenesis of gastric cancer cell line BGC823

TAN Bi-bo, LI Yong, FAN Li-qiao, ZHAO Qun, WANG Dong, LIU Yu   

  1. The Third Department of Surgery, the Fourth Affiliated Hospital, Hebei Medical University, Shijiazhuang Hebei 050011, China
  • Published:2014-12-30 Online:2015-05-07
  • Contact: LI Yong E-mail: li_yong_hbth@126.com

摘要: 背景与目的:研究发现Vav3基因在多种恶性肿瘤中表达异常,但Vav3与胃癌血管生成的关系尚不明确。本研究通过抑制内源性Vav3,观察其对胃癌细胞血管生成基因表达的影响,并探讨其机制和意义。方法:荧光定量RT-PCR及蛋白质印迹法(Western blot)检测人胃癌细胞株BGC823、胃上皮细胞株GES-1中Vav3的表达;合成针对Vav3的小干扰RNA(small interference RNA,siRNA),并转染胃癌细胞株BGC823;MTT法检测转染前后胃癌细胞的活性;检测转染前后BGC823血管生成相关基因血管内皮生长因子-A(vascular endothelial growth factor-A,VEGF-A)、VEGF-C、VEGF-D、血管生成素-2(angiogenin-2,Ang-2)、血管生成抑制蛋白-1(vasohibin-1)表达的变化。结果:Vav3在胃癌BGC823细胞中的表达明显高于胃上皮细胞株GES-1(P<0.01);Vav3-siRNA转染BGC823细胞后,Vav3表达明显受到抑制(P均<0.01);MTT结果显示Vav3-siRNA转染后,BGC823活性明显降低(P<0.05);转染后B G C 8 2 3 中VEGF-C和Ang-2表达均较转染前降低(P均<0 . 0 5 ) , 而vasohibin-1表达则升高(P均<0.05)。结论:Vav3对部分胃癌细胞血管生成相关基因有调控作用,并可能通过这种作用促进肿瘤血管生成。

关键词: 胃癌, Vav3基因, 血管生成, RNA干扰

Abstract: Background and purpose: It was reported that Vav3 gene was expressed aberrantly in many cancers. But the relationship between Vav3 and angiogenesis genes of gastric cancer is still not clear. The purpose of this research was to investigate the effect and significance of Vav3 to angiogenesis of human gastric cancer cell line BGC823. Methods: The expressions of Vav3 in human gastric cancer cell line BGC823, gastric epithelial cell line GES-1 were tested by fluorecence quantitative RT-PCR and Western blot. Then Vav3-siRNA was synthesized and transfected into BGC823. Activity of BGC823 was measured with fluorecence quantitative RT-PCR and MTT assay. The expressions of angiogenesis related genes VEGF-A, VEGF-C, VEGF-D, angiogenin-1 (Ang-2), vasohibin-1 were determined by qPCR and Western blot. Results: Expressions of Vav3 were detected higher in gastric cancer BGC823 cells than in GES-1 (P<0.01). Expression of Vav3 was inhibited by Vav3-siRNA (P<0.05). Activity of BGC823 was obviously inhibited after Vav3-siRNA transfected with MTT assay (P<0.05). The expressions of VEGF-C, Ang-2 were lower in cells after transfected by Vav3-siRNA(both P<0.05); expression of Vasohibin-1 increased after Vav3-siRNA transfected into BGC823 (P<0.05). Conclusion: Vav3 gene can regulate some angiogenesis related genes, and Vav3 may promote angiogenesis of gastric cancer cells with this fuction.

Key words: Gastric cancer, Vav3 gene, Angiogenesis, RNA interference