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The roles of adhesion molecule and cytokine in cancer metastasis

粘附分子和细胞因子在癌症转移中的作用

基本信息

批准号：
07671303
负责人：
MURATA Atsuo
金额：
$ 1.47万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

项目摘要

1)B 16 mouse melanoma cells were much more adhered to vascular to vascular endothelial cells stimulated by interleukin-1 (IL-1). Since the adhesion was inhibited by antiintegrin a4 subunit antibody or vascular cell adhesion-1 (VCAM-1), integrin a4b1 on B16 cells was supposed to be interacted with VCAM-1 on endothelial cells. The effect of IL-1 was examined in lung metastasis of B 16 cells in mouse. Pretreatment of IL-1 increased lung metastasis more frequently and the lung metastasis was blocked by anti-a4 antibody. Together with the in vitro results, pretreatment of IL-1 induced VCAM-1 on endothelial cells and potentiated lung metastasis of B 16 cells expressing a4b1.2)The roles of adhesion molecule and cytokine were examined in organ specific metastasis. MAG cells, established from pleural effusion of the patient with esophageal cancer, were inoculated into foot pad, tail vein, or spleen of the nude mice. Metastases in the lymph node, lung, or liver were observed respectively. When cultured cells from metastatic foci were reinjected, each metastasis was observed more quickly. High metastatic cells were established respectively to lymph node, lung or liver after the procedures were performed 5 times. Growth rate, adhesion to extracellular matrix, cell migration, cell invasion to Matrigel, expression of integrin molecules and secretion of cytokine were examined in these high metastatic cells. As a result, each high metastatic cell decreased growth rate but increased cell adhesion, migration and invasion significantly. These changes were associated with expression of integrin on cells and secretion of cytokine.These data suggested expression of integrin molecules and secretion of cytokine play some roles in cancer metastasis and organ specific metastasis.

1）白细胞介素1（IL-1）刺激后，B 16小鼠黑色素瘤细胞与血管内皮细胞的粘附明显增强。由于B16细胞表面的整合素α 4亚单位抗体或血管细胞粘附分子1（VCAM-1）可抑制B16细胞表面的整合素α 4 β 1与内皮细胞表面的VCAM-1相互作用。观察IL-1对小鼠B 16细胞肺转移的影响。IL-1预处理可增加肺转移，抗α 4抗体可阻断肺转移。结合体外实验结果，IL-1预处理诱导内皮细胞VCAM-1表达，增强表达α 4 β 1的B 16细胞的肺转移。2）粘附分子和细胞因子在器官特异性转移中的作用。将从食管癌患者胸腔积液中建立的MAG细胞接种到裸鼠的足垫、尾静脉或脾脏中。分别观察到淋巴结、肺或肝转移。当从转移灶培养的细胞被重新注射时，每个转移被更快地观察到。5次后分别在淋巴结、肺和肝建立高转移细胞。检测这些高转移细胞的生长速度、细胞与细胞外基质的粘附、细胞迁移、细胞对Matrigel的侵袭、整合素分子的表达和细胞因子的分泌。结果，每个高转移细胞的生长速度下降，但增加细胞粘附，迁移和侵袭显着。这些变化与细胞表面整合素的表达和细胞因子的分泌有关，提示整合素分子的表达和细胞因子的分泌在肿瘤转移和器官特异性转移中起一定作用。