Vascular endothelial growth factor receptor-2 or
kinase insert domain-containing receptor (VEGFR2/KDR) is secreted by most solid
tumors, including
breast cancer, and is an important mediator of angiogenesis. To observe the effects of KDR gene expression on cell proliferation and the cell cycle in MCF-7 cells in vitro and in vivo, we used chemically modified
siRNA directed against KDR. The results revealed that chemically modified
siRNA transfection of the KDR gene effectively inhibited the proliferation of MCF-7 cells, arrested cells in the G1 phase and down-regulated the expression of KDR. In addition, in the progression of cell cycle arrest induced by
siRNA, phosphorylated ERK and CDK1 expression was down-regulated (P<0.01). In vivo, the growth of
tumors was visibly suppressed. RT-PCR and the results of immunohistochemistry indicated that KDR
mRNA and
protein expression was reduced in the excised
tumors. In contrast, there were no obvious changes in the control groups. This implies that chemically modified KDR
siRNA markedly decreases KDR gene expression and inhibits cellular proliferation in vitro, as well as suppressing
tumor growth in a xenograft model. KDR may be a new target for
breast cancer treatment.