ABSTRACT
Vascular endothelial growth factor 165 (VEGF165)-mediated autocrine stimulation of tumor cells enhances the progression to a malignant phenotype.VEGF165b competes with VEGF165 and binds to vascular endothelial growth factor receptor (VEGFR),resulting in inhibition of downstream signal transduction pathways.This study was designed to investigate the role of VEGF165b in the migration and invasion of human lung adenocarcinoma A549 cells.The full-length of VEGF165b was constructed and cloned into an expression plasmid (pVEGF165b),and then transfected into A549 cells.Dimethylthiazolyl-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect the effect of VEGF165b on proliferation of transfected cells.Reverse transcription polymerase chain reaction (RT-PCR) was employed to examine the effect of VEGF165b on the expression of VEGF165 in transfected cells.Wound-healing assays were used to investigate the effect of VEGF165b on migration of transfected cells.Matrix metalloproteinase (MMPs) activity assay and in vitro invasion assay were used to determine the role of VEGF165b in invasion of transfected cells.There was no significant change in proliferation of A549 cells after transfection of pVEGF165b,but the expression of VEGF165,migration and invasion in A549 cells were inhibited.Furthermore,exogenous VEGF165b inhibited the activity of MMP9 in the supematant of A549 cells and the subsequent invasion capacity of those cells.We therefore conclude that exogenous VEGF165b can inhibit the expression of VEGF165,as well as the migration and invasion ofA549 cells,but has no effect on the proliferation ofA549 cells.
ABSTRACT
is and K-ras mutation. It was concluded that aberrant methylation of the RASSF2A gene with the subsequent loss of RASSF2A expression plays an important role in the pathogenesis of HCC.