Abstract
BackgroundHere we aimed to investigate the effect of COX-2 siRNA on proliferation and angiogenesis of gastric cancer cells.MethodsThe gastric cancer cell line SGC7901 was transfected with COX-2 siRNA, then the growth and angiogenesis of cells were detected by in vitro and in vivo assay. Human microarray, RT-PCR and western blot were used to identify differentially expressed angiogenesis-related molecules in cells with decreased expression of COX-2.ResultsDown-regulation of COX-2 could significantly inhibit the in vitro and in vivo growth of gastric cancer cells, and suppress the migration and tube formation of human umbilical vein endothelial cells. Totally 23 angiogenesis-related molecules were found involved in COX-2-induced angiogenesis suppression. The results of RT-PCR and western blot showed that down-regulation of COX-2 might inhibit VEGF, Flt-1, Flk-1/KDR, angiopoietin-1, tie-2, MMP2 and OPN.ConclusionsCOX-2 might mediate tumor angiogenesis and growth, and could be considered as a target for gastric cancer therapy.
Highlights
We aimed to investigate the effect of COX-2 siRNA on proliferation and angiogenesis of gastric cancer cells
Down-regulation of COX-2 inhibited angiogenesis of gastric cancer cells As shown in Figure 3, the number of endothelial cells within the tumors formed by COX-2-downregulating cells was less than that of tumors formed by control cells
In order to investigate the angiogenic property of COX-2 in endothelial cells, the in vitro tube formation of HUVEC was assessed
Summary
We aimed to investigate the effect of COX-2 siRNA on proliferation and angiogenesis of gastric cancer cells. The treatment outcome of this common malignancy is still not satisfactory and various chemotherapeutic attempts in an adjuvant setting have failed to improve the survival rate in gastric cancer. Angiogenesis has been found related to hematogenous recurrence and poor prognosis in gastric cancer [1]. Angiogenesis is the growth of new vessels from existing vasculature. A balance of angiogenic and angiostatic growth factors tightly controls physiological angiogenesis. Tipping of this balance towards a pro-angiogenic environment is termed the ‘angiogenic switch’ and occurs in situations such as tissue hypoxia, inflammation or neoplasia [2]
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