抽象
细胞间粘附分子-1(ICAM-1)表达的肿瘤细胞可能参与在其与防御细胞的相互作用。在这项研究中的表面ICAM-1表达和可溶性ICAM-1(sICAM-1的)的生产通过五个小细胞肺癌(SCLC)和5个非SCLC(NSCLC)细胞系进行了研究。此外,ICAM-1上调通过对肺癌细胞的粘附到同种异体淋巴因子激活的杀伤(LAK)细胞和易感性LAK细胞毒性的细胞因子的影响也进行了评价。ICAM-1的表达,通过流式细胞术评估。可溶性ICAM-1释放通过酶联免疫吸附测定(ELISA)进行测定。与LAK细胞相互作用通过粘附和细胞毒性测定法进行测试。在基线时,SCLC线不表达ICAM-1,而4 5 NSCLC系中表达ICAM-1。ICAM-1的表达在5条SCLC线4诱导干扰素-γ(IFN-γ),并在5条NSCLC线1上调。ICAM-1的表达在5条SCLC线(美国国家癌症研究所(NCI)H211)的1诱导的肿瘤坏死因子-α(TNF-α),和上调在5条NSCLC线(NCI H460和NCI H838)的2-。在后者中的线条,一个(NCI H838)公布显著量sICAM-1的的。 Adhesion to LAK cells and susceptibility to LAK cytotoxicity were significantly higher in TNF-alpha-treated NCI H460 and NCI H211 cells, compared to untreated NCI H460 and NCI H211 cells. In contrast, no difference in adhesion to LAK cells and susceptibility to LAK cytotoxicity was detected between baseline and TNF-alpha-treated NCI H838 cells. Intercellular adhesion molecule-1 surface expression and soluble intercellular adhesion molecule-1 release may play an important role in interactions between lymphokine-activated killer cells and lung cancer cells.