基质细胞衍生因子-1(SDF-1)和CXC趋化因子受体4(CXCR4)受血管内皮生长因子(VEGF)上调,并促进胶质瘤细胞侵袭。

SDF-1 and CXCR4 are up-regulated by VEGF and contribute to glioma cell invasion.

作者信息

Hong Xin, Jiang Feng, Kalkanis Steven N, Zhang Zheng Gang, Zhang Xue-Peng, DeCarvalho Ana C, Katakowski Mark, Bobbitt Kevin, Mikkelsen Tom, Chopp Michael

机构信息

Department of Neurosurgery, Henry Ford Heath Science Center, Detroit, MI 48202, USA.

出版信息

Cancer Lett. 2006 May 8;236(1):39-45. doi: 10.1016/j.canlet.2005.05.011. Epub 2005 Jun 20.

Abstract

Glioma cells produce vascular endothelial growth factor (VEGF) to induce vascularization and thereby supply the malignant tissue with oxygen and nutrients. However, little is known about the direct effects of VEGF on tumor cells. In this study, we investigate the ability of VEGF to promote proliferation and invasion of human glioma cells (U251n). Since the chemokine and its receptor, SDF-1/CXCR4, promote glioma cell proliferation and are up-regulated in human glioblastomas, we also tested the effects of VEGF on SDF-1 and CXCR4 mRNA expression. Using cell culture, the effect of VEGF on proliferation of U251n cells was measured using ELISA to detect incorporated BrdU as a marker of DNA syntheses. The effects of VEGF and SDF-1 on U251n cell invasion and proliferation were measured using inhibitors to VEGF receptor1 and receptor2, DC101 and MF1, respectively, and a CXCR4 antagonist (AMD3100). SDF-1 and CXCR4 mRNA expression in U251n and U87MG cells were measured using quantitative PCR. VEGF antisense phosphorothioate oligodeoxynucleotide (AS-VEGF) was also used to down-regulate VEGF expression in U251n cells. VEGF significantly increased U251n cell proliferation and invasion in a dose-dependent manner. These effects were blocked by the VEGF receptor inhibitors, DC101/MF1. The CXCR4 antagonist AMD3100 blocked U251n increased invasion, but not proliferation. CXCR4 and SDF-1 mRNA were up-regulated when U251n and U87MG cells were treated with VEGF. Eight micrometer VEGF antisense phosphorothioate oligodeoxynucleotide (AS-VEGF) down-regulated CXCR4 and SDF-1 mRNA levels in U251n cells. VEGF has a direct effect on U251n glioma cell proliferation and invasion. VEGF up-regulates SDF-1 and CXCR4 mRNA expression, and contributes to U251n cell invasion.

摘要

胶质瘤细胞产生血管内皮生长因子(VEGF)以诱导血管生成,从而为恶性组织提供氧气和营养物质。然而,关于VEGF对肿瘤细胞的直接作用知之甚少。在本研究中,我们调查了VEGF促进人胶质瘤细胞(U251n)增殖和侵袭的能力。由于趋化因子及其受体SDF-1/CXCR4促进胶质瘤细胞增殖且在人胶质母细胞瘤中上调,我们还测试了VEGF对SDF-1和CXCR4 mRNA表达的影响。使用细胞培养,通过酶联免疫吸附测定(ELISA)检测掺入的BrdU作为DNA合成标志物来测量VEGF对U251n细胞增殖的影响。分别使用VEGF受体1和受体2的抑制剂DC101和MF1以及CXCR4拮抗剂(AMD3100)来测量VEGF和SDF-1对U251n细胞侵袭和增殖的影响。使用定量PCR测量U251n和U87MG细胞中SDF-1和CXCR4 mRNA的表达水平。VEGF反义硫代磷酸酯寡脱氧核苷酸(AS-VEGF)也用于下调U251n细胞中的VEGF表达。VEGF以剂量依赖性方式显著增加U251n细胞的增殖和侵袭。这些作用被VEGF受体抑制剂DC101/MF1阻断。CXCR4拮抗剂AMD3100阻断了U251n细胞侵袭的增加,但未阻断增殖。当用VEGF处理U251n和U87MG细胞时,CXCR4和SDF-1 mRNA上调。8μm的VEGF反义硫代磷酸酯寡脱氧核苷酸(AS-VEGF)下调了U251n细胞中CXCR4和SDF-1 mRNA的水平。VEGF对U251n胶质瘤细胞的增殖和侵袭有直接作用。VEGF上调SDF-1和CXCR4 mRNA表达,并促进U251n细胞侵袭。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索