| Background:Glioma derived from a variety of neuroectodermal glial cell line, is the mostcommon intracranial tumor, more than half of which is malignant and easy to relapse.Gliomas are difficult to eradicate, in particular pleomorphic glioblastoma with richblood supply, and become a major clinical problem.Vascular endothelial growthfactor , VEGF, is found in the role of the strongest and highest specificity to promotethe growth of tumor angiogenesis factor.VEGF and its receptors regulates endothelialcell differentiation and angiogenesis through paracrine way[1].For VEGFR-2 is one ofthe high-affinity VEGF receptor, a number of studies point out its high level ofexpression is related with the rich angiogenesis in glioma[2].Objective:All of previous studies of endothelial cells are just for VEGFR-2 receptorexpression.This study is for the VEGFR-2 receptor-positive glioma cell, and for itsrole in glioma. Hong et al[3] has proved that U87 cells expressed VEGFR-2. VEGFR-2 (+) U87 cells were chosen as the research objector in this test to explore their ownexpression of VEGFR-2 in glioma cell on the impact of its own growth, apoptosis,proliferation and invasion.Methods:VEGFR-2 siRNA was synthesized and transfected into U87 cells, and selectedthe most effective VEGFR-2 siRNA by real-time quantitative PCR, and verified byWestern Blot. The apoptosis, invasion and proliferation of transfected U87 cells wereevaluated via Flow cytometric method, Transwell, MTT, and Fluorescence Microscope.ResultsResults:The most effective VEGFR-2 siRNA was successfully screened and transfectedinto U87 cells in vitro. VEGFR-2 siRNA leads to U87 cells growth suppression,invasion reduction, but not apoptosis increase, compared with the negative controlgroup and the control group.Conclusions:Inhibiting the self-expression VEGFR-2 of U87 cells could effectively inhibitthe cells U87 growth and reduce invasion... |
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