Okahara H, Yagita H, Miyake K, Okumura K
First Department of Surgery, School of Medicine, Juntendo University, Tokyo, Japan.
Cancer Res. 1994 Jun 15;54(12):3233-6.
In this study, we examined the effect of tumor necrosis factor alpha (TNF-alpha) on pulmonary metastasis of murine melanoma B16-BL6 by focusing on the intercellular adhesion molecules involved in the metastatic process. TNF-alpha administration before B16-BL6 inoculation significantly enhanced the experimental pulmonary metastasis. The enhancement was seen when TNF-alpha was administered 4 h, but not 24 h, before B16-BL6 inoculation. Administration of 50-5000 units of TNF-alpha increased the number of metastatic lung colonies in a dose-dependent manner. Flow cytometric analysis demonstrated a high expression of very late activation antigen 4 (VLA-4) on the surface of B16-BL6 cells. Immunoperoxidase staining demonstrated that a ligand for VLA-4, vascular cell adhesion molecule 1, was expressed on lung vascular endothelium 4 h after administration of TNF-alpha. Pretreatment of B16-BL6 cells with an anti-VLA-4 monoclonal antibody abolished the TNF-alpha-enhanced pulmonary lung colonies. Administration of an anti-vascular cell adhesion molecule 1 monoclonal antibody also abolished the enhancement. These results indicate that the interaction between VLA-4 on tumor cells and vascular cell adhesion molecule 1 on activated endothelial cells is critically involved in TNF-alpha enhancement of metastasis.
在本研究中,我们通过关注转移过程中涉及的细胞间黏附分子,研究了肿瘤坏死因子α(TNF-α)对小鼠黑色素瘤B16-BL6肺转移的影响。在接种B16-BL6之前给予TNF-α可显著增强实验性肺转移。当在接种B16-BL6前4小时而非24小时给予TNF-α时,可观察到这种增强作用。给予50 - 5000单位的TNF-α可使肺转移瘤集落数量呈剂量依赖性增加。流式细胞术分析显示B16-BL6细胞表面非常晚期活化抗原4(VLA-4)高表达。免疫过氧化物酶染色显示,在给予TNF-α 4小时后,肺血管内皮细胞上表达VLA-4的配体血管细胞黏附分子1。用抗VLA-4单克隆抗体预处理B16-BL6细胞可消除TNF-α增强的肺转移瘤集落。给予抗血管细胞黏附分子1单克隆抗体也可消除这种增强作用。这些结果表明,肿瘤细胞上的VLA-4与活化内皮细胞上的血管细胞黏附分子1之间的相互作用在TNF-α增强转移中起关键作用。