Effects of endostatin on the growth and lymphangiogenesis of Lewis lung carcinoma xenograft in mice

Abstract

to investigate the effects of endostar, a recombined humanized endostatin, on the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenograft in mice. lewis lung carcinoma (LLC) xenograft were established in C57 mice by intravenous transplantation of 1 × 10(6) cells. Then tumor-bearing mice were assigned into two groups: control group received caudal vein injections of 0.2 ml of 0.9% sodium chloride for 15 days, and treatment group received 500 µg endostar daily. Six weeks after LLC cell injection mice were sacrificed, and then tumor numbers and size were recorded. The expression of vascular endothelial growth factor-c (VEGF-C) and microlymphatic vessel density (MLVD) were observed by immunohistochemical staining. tumor number and size of control group were significantly higher than those of treatment group. The microlymphatic vessel density (MLVD) was 5.7 ± 1.6 in the treatment group, which was markedly lower than in the control mice (7.8 ± 1.6). Two lymph node metastases were observed in treatment group, and eight in control group. Lymphatic metastases were more frequent in control group than in treatment group. Expression of VEGF-C in control group was significantly higher than that in treatment group. endostar significantly inhibits the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenografts, and the inhibitory effect is due to its ability to regulate the expression of VEGF-C of tumors in part.