c-Met-targeted RNA interference inhibits growth and metastasis of glioma U251 cells in vitro

被引：36

作者：

Chu, Sheng-Hua ^{[1
,2
]}

Feng, Dong-Fu ^{[1
,2
]}

Zhang, Hong ^{[1
,2
]}

Chen, Er-Tao ^{[1
,2
]}

Duan, Zhi-Xin ^{[1
,2
]}

Li, Xue-Yuan ^{[1
,2
]}

Li, Jia ^{[1
,2
]}

Ma, Yan-Bin ^{[1
,2
]}

Zhu, Zhi-An ^{[1
,2
]}

Qiu, Jian-Hua ^{[1
,2
]}

机构：

[1] 3 Peoples Hosp Affiliated Shanghai Jiao Tong Univ, Dept Neurosurgery, Shanghai 201900, Peoples R China

[2] Shanghai Jiao Tong Univ, Sch Med, People Hosp Affiliated 3, Dept Neurosurg, Shanghai 201900, Peoples R China

来源：

JOURNAL OF NEURO-ONCOLOGY | 2009年 / 93卷 / 02期

关键词：

c-Met; Apoptosis; Adherence; Gene therapy; Glioma; RNA interference; FACTOR RECEPTOR; CARCINOMA; LINES; PROLIFERATION; ANGIOGENESIS; MESOTHELIOMA; EXPRESSION; SECRETION; RADIATION; MIGRATION;

D O I：

10.1007/s11060-008-9772-5

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Angiogenesis plays an essential role in tumor growth and metastasis and is a promising target for cancer therapy. c-Met, a receptor tyrosine kinase, and its ligand, hepatocyte growth factor (HGF), are critical in cellular proliferation, motility, invasion, and angiogenesis. The present study was designed to determine the role of c-Met in growth and metastasis of glioma U251 cells using RNA interference (RNAi) technology in vitro. We constructed three kinds of shRNA expression vectors aiming at the c-Met gene, then transfected them into glioma U251 cells by lipofectamine(TM) 2000. The level of c-Met mRNA was investigated by real-time polymerse chain reaction (RT-PCR). The protein expression of c-Met was observed by immunofluoresence staining and western blotting. U251 cell growth and adherence was detected by methyl thiazole tetrazolium assay. The apoptosis of U251 cells was examined with a flow cytometer. The adherence, invasion, and in vitro angiogenesis assays of U251 cells were done. We got three kinds of c-Met specific shRNA expression vectors which could efficiently inhibit the growth and metastasis of U251 cells and the expression of c-Met in U251 cells. RT-PCR, immunofluoresence staining and western blotting showed that inhibition rate for c-Met expression was up to 90%, 79% and 85%, respectively. The expression of c-Met can be inhibited by RNA interference in U251 cells, which can inhibit the growth and metastasis of U251 cell and induce cell apoptosis. These results indicate that RNAi of c-Met can be an effective antiangiogenic strategy for glioma.

引用

页码：183 / 189

页数：7

共 28 条

[1] Insulinlike growth factor-I-mediated migration and invasion of human colon carcinoma cells requires activation of c-Met and urokinase plasminogen activator receptor [J].