Effect of AMD3100 on the proliferation and angiogenesis of AsPC-1 cells
10.3760/cma.j.issn.1674-1935.2010.05.010
- VernacularTitle:AMD3100对胰腺癌细胞AsPC-1及其移植瘤血管生成的影响
- Author:
Zhenjun GAO
;
Qingyun KONG
;
Kai WU
;
Xingpeng WANG
- Publication Type:Journal Article
- Keywords:
Pancreatic neoplasms;
AMD3100;
Cell proliferation;
Angiogenesis
- From:
Chinese Journal of Pancreatology
2010;10(5):335-337
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of blockade on non-peptide specific SDF-1/CXCR4 receptor ligand system with AMD3100 on the proliferation and angiogenesis of human pancreatic cancer cells AsPC-1. Methods AsPC-1 was divided into control group, SDF-1α group, group, SDF-1α + AMD3100 group. MTT test was performed to determine the proliferative level of AsPC-1 cells. Vascular endothelial growth factor (VEGF) was detected with Western blotting assay. Immunohistochemistry was used to detect the microvessel density (MVD) in subcutaneous xenografts of AsPC 1 of nude mice model, which was intratumorally and peritumorally injected with AMD3100. Results SDF-1α could induce the proliferation of AsPC-1(1.430 ±0. 122 vs 1. 002 ± 0. 001, P <0. 05). While the proliferative effect induced by SDF-1α could be inhibited by AMD3100 (0.983 ±0. 068vs 1.430 ± 0. 122, P <0.05). SDF-1α could induce the expression of VEGF (0. 565 ± 0. 047 vs 0. 439 ± 0.034, P < 0.05). While the protein expression of VEGF induced by SDF-1α on AsPC-1 cells was inhibited by AMD3100 (0. 450 ± 0. 071 vs 0. 565 ± 0. 04, P <0. 05). The growth and angiogenesis of subcutaneous xenografts of nude mice model were inhibited by AMD3100; the tumor inhibitory rate was 59. 5% at 24th day. The MVD of xenografts was significantly decreased (28.56 ± 6.94 vs 98.75 ± 20. 60, P < 0. 01 ). Conclusions AMD3100 could inhibit the proliferation and angiogenesis of AsPC-1 cells both in vitro and in vivo.
