Yudoh K, Matsui H, Tsuji H
Department of Orthopaedic Surgery, Toyama Medical and Pharmaceutical University, Japan.
Clin Exp Metastasis. 1997 Nov;15(6):557-67. doi: 10.1023/a:1018487213157.
Human fibrosarcoma HT1080 cell surface phenotype analysis revealed the expression of "cluster of differentiation 15" (CD15) antigen and to a lesser extent, of "very late antigen-4" (VLA-4). Expression of "endothelial-leukocyte adhesion molecule-1" (ELAM-1) was negligible on resting human umbilical vascular endothelial cells (HUVECs), but its expression could be induced by HT1080 conditioned medium. HT1080 cell adhesion to HUVECs was partially dependent on CD15/ELAM-1 adhesion molecules. HT1080 cell adhesion to HUVECs induced the enhancement of nitric oxide (NO) production from HUVECs. Exogenous NO and NO from HUVECs enhanced ELAM-1 expression on HUVECs, HT1080 cell adhesion to HUVECs, permeability of the HUVEC monolayer, and HT1080 cell invasion through the HUVEC monolayer. These enhancements were not induced by NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME). These results suggest that NO expression induced by tumor cells via the CD15/ELAM-1 adhesion system may contribute to enhancement of tumor cell adhesion to endothelial cells and hyperpermeability of the endothelium, facilitating tumor cell invasion.
人纤维肉瘤HT1080细胞表面表型分析显示“分化簇15”（CD15）抗原的表达，以及程度较低的“极迟抗原-4”（VLA-4）的表达。“内皮细胞-白细胞黏附分子-1”（ELAM-1）在静息人脐静脉血管内皮细胞（HUVECs）上的表达可忽略不计，但其表达可被HT1080条件培养基诱导。HT1080细胞与HUVECs的黏附部分依赖于CD15/ELAM-1黏附分子。HT1080细胞与HUVECs的黏附诱导了HUVECs一氧化氮（NO）产生的增强。外源性NO和来自HUVECs的NO增强了HUVECs上ELAM-1的表达、HT1080细胞与HUVECs的黏附、HUVEC单层的通透性以及HT1080细胞穿过HUVEC单层的侵袭。这些增强作用不是由一氧化氮合酶抑制剂N（G）-硝基-L-精氨酸甲酯（L-NAME）诱导的。这些结果表明，肿瘤细胞通过CD15/ELAM-1黏附系统诱导的NO表达可能有助于增强肿瘤细胞与内皮细胞的黏附以及内皮的高通透性，促进肿瘤细胞侵袭。
