Ruco L P, de Laat P A, Matteucci C, Bernasconi S, Sciacca F M, van der Kwast T H, Hoogsteden H C, Uccini S, Mantovani A, Versnel M A
Dipartimento di Medicina Sperimentale e Patologia, Università La Supienza, Roma, Italy.
J Pathol. 1996 Jul;179(3):266-71. doi: 10.1002/(SICI)1096-9896(199607)179:3<266::AID-PATH592>3.0.CO;2-Y.
Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are cytokine-inducible adhesion molecules which recognize ligands that are highly expressed on leukocytes. Expression of ICAM-1 and VCAM-1 was investigated in tissue sections of 16 cases of malignant mesothelioma (seven epithelial, eight biphasic, and one sarcomatoid) using immunohistochemistry. Neoplastic cells were diffusely and intensely stained for ICAM-1 in all cases. VCAM-1 was detected in 14 of 16 cases. The percentage of VCAM-1-positive tumour cells was more than 50 per cent in eight cases and the staining was observed mainly in epithelial-like cells. VCAM-1 was rarely expressed in other malignant tumours of epithelial origin, being present in only 1 of 58 cases of carcinoma originating from different anatomical sites. At the cellular level, ICAM-1 and VCAM-1 appeared co-distributed, the staining for both being cytoplasmic with a membrane reinforcement. The regulation of VCAM-1 expression by neoplastic mesothelial cells was investigated in vitro using 14 mesothelioma cell lines. ICAM-1 was expressed by cultured cells of all mesothelioma cell lines, even in the absence of cytokines. VCAM-1 was detected in 10-50 per cent of the cells in three non-stimulated mesothelioma cell lines (mero-95, mero-96, and mero-134), and was absent or poorly expressed in the remaining 11. Exposure of a negative cell line (mero-48a) to an optimal concentration of tumour necrosis factor alpha (TNF alpha) or interleukin-13 (IL-13) for 6-18 h resulted in the induction of VCAM-1 mRNA synthesis and in VCAM-1 expression at the membrane level in 60-70 per cent of the cells. These findings are consistent with the possibility that TNF alpha, IL-13, or other activating signals are released in the tumour micro-environment and regulate the expression of VCAM-1 in malignant mesothelioma cells.
细胞间黏附分子-1（ICAM-1）和血管细胞黏附分子-1（VCAM-1）是细胞因子诱导的黏附分子，可识别在白细胞上高度表达的配体。采用免疫组织化学方法，对16例恶性间皮瘤（7例上皮型、8例双向型和1例肉瘤样型）组织切片中ICAM-1和VCAM-1的表达进行了研究。所有病例中肿瘤细胞均弥漫性、强阳性表达ICAM-1。16例中有14例检测到VCAM-1。8例中VCAM-1阳性肿瘤细胞百分比超过50%，染色主要见于上皮样细胞。VCAM-1在其他上皮源性恶性肿瘤中很少表达，58例来自不同解剖部位的癌中仅1例出现表达。在细胞水平上，ICAM-1和VCAM-1似乎共分布，两者染色均位于细胞质且有膜增强。利用14种间皮瘤细胞系在体外研究了肿瘤性间皮细胞对VCAM-1表达的调节。所有间皮瘤细胞系的培养细胞均表达ICAM-1，即使在无细胞因子的情况下也是如此。在3种未刺激的间皮瘤细胞系（mero-95、mero-96和mero-134）中，10%-50%的细胞检测到VCAM-1，其余11种细胞系中未检测到或表达较弱。将阴性细胞系（mero-48a）暴露于最佳浓度的肿瘤坏死因子α（TNFα）或白细胞介素-13（IL-13）6-18小时，导致60%-70%的细胞中VCAM-1 mRNA合成诱导及膜水平VCAM-1表达。这些发现与肿瘤微环境中释放TNFα、IL-13或其他激活信号并调节恶性间皮瘤细胞中VCAM-1表达的可能性一致。
