Tamaki M, Aoyagi M, Morita I, Hirakawa K, Murota S
Department of Neurosurgery, Graduate School, Tokyo Medical & Dental University, Japan.
J Neurooncol. 1995;24(2):181-8. doi: 10.1007/BF01078488.
The interactions between tumor cells and endothelium play a key role in the process of tumor growth, local invasion, and distant metastasis. In the present study, we examined the adhesion of C6 glioma cells to bovine endothelial cell (EC) monolayers and defined the cell adhesion molecules acting between these cells. Pretreatment of the EC monolayer with cytokines, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and interferon (INF)-gamma, significantly increased the adhesion of C6 glioma cells to the EC monolayer. The effect lasted more than 24 hours and was protein-synthesis dependent. The adhesion of C6 glioma cells to TNF-activated ECs was blocked by the monoclonal antibody to the intercellular adhesion molecule-1 (ICAM-1) or beta 2 integrin, whereas that of melanoma cells was not. These findings provide evidence that ICAM-1 and beta 2 integrin function as inducible cell surface molecules that can support the adhesion of C6 glioma cells to ECs, and may contribute to the characteristic growth of glial tumors in vivo.
肿瘤细胞与内皮细胞之间的相互作用在肿瘤生长、局部侵袭和远处转移过程中起着关键作用。在本研究中,我们检测了C6胶质瘤细胞与牛内皮细胞单层的黏附情况,并确定了这些细胞之间起作用的细胞黏附分子。用细胞因子、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和干扰素(INF)-γ预处理内皮细胞单层,可显著增加C6胶质瘤细胞与内皮细胞单层的黏附。该效应持续超过24小时,且依赖于蛋白质合成。C6胶质瘤细胞与TNF激活的内皮细胞的黏附被抗细胞间黏附分子-1(ICAM-1)或β2整合素的单克隆抗体阻断,而黑色素瘤细胞则不然。这些发现提供了证据,表明ICAM-1和β2整合素作为可诱导的细胞表面分子,能够支持C6胶质瘤细胞与内皮细胞的黏附,并可能有助于体内胶质肿瘤的特征性生长。