摘要
目的探讨RNA干扰（RNAi）抑制信号传导与转录激活因子3（STAT3）对人胰腺癌体外血管生成的影响及其机制。方法RNAi抑制胰腺癌细胞株SW1990细胞中STAT3、噻唑蓝（MrIT）和流式细胞技术分别检测胰腺癌细胞上清液对人脐静脉内皮细胞（HUVEC）细胞增殖和细胞周期的影响。体外迁移实验检测胰腺癌细胞上清液诱导的HUVEC迁移能力；酶联免疫吸附试验（ELISA）检测胰腺癌细胞L清液中血管内皮生长因子（VEGF）蛋白表达。结果MTT和流式细胞仪结果显示RNAi抑制STAT3后，HUVEC增殖能力下降，24．48、72h的细胞增殖率分别为（1．19±0．11）％、（1．62±0．15）％、（1．95±0．18）％；细胞周期阻滞于G0／G。期，为（80．95±7．49）％。体外迁移实验显示RNAi抑制STAT3后，HUVEC迁移能力明显减弱。ELISA显示RNAi抑制STAT3后，VEGF蛋白表达下降60％。结论RNAi抑制STAT3可以通过下调VEGF，抑制胰腺癌细胞体外血管生成能力。
Objective To investigate the effect and mechanism of RNA interference （RNAi）-mediated signal transducer and activator of transcription 3 （STAT3） inhibition on human pancreatic cancer cells angiogenesis in vitro. Methods RNAi was used to inhibit STAT3 gene of SW1990 ceils. Methyl thi7 azol tetrazolium （MTF） assay and flow cytometric analysis were performed to detect cell proliferation and cell cycle of human umbilical vein endothelial cell （HUVEC） , respectively. The migration ability of HU- VECs was determined by cell migration assay. Enzyme linked immunosorbent assay （ELISA） was used to detect the protein expression of the vascular endothelial growth factor （VEGF）, Results Inhibition Of STAT3 with RNAi significantly inhibited the proliferation of HUVECs and decreased the migration ability of ltUVECs in vitro. The cell growth rate at 24, 48, 72 h in SW1990-RNAi group was （ 1.19±0. 11 ） % , （1. 62 ± 0. 15 ）%, （1. 95 ±0. 18）%, respectively. The percentage of HUVECs at G0/G1 phaSe in SW1990-RNAi group was （80. 95 ±7.49） %. Moreover, the VEGF protein expression in SW1990-RNAi cells was 1educed by 60%. Conclusion Inhibition of STAT3 with RNAi can significantly inhibit the angiogenesis ability of pancreatic cancer cells through down-regulating VEGF, which may provide a novel strategy in preventing the angiogenesis of pancreatic cancer.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2012年第1期16-18,共3页
Chinese Journal of Experimental Surgery
基金
上海市科学技术委员会青年科技启明星项目（09QA14-04600）
关键词
RNA干扰
信号传导与转录激活因子3
胰腺癌
血管生成
RNA interference
SignaI transducer and activator of transcription 3
Pancreatic carcinoma
Angiogenesis
