Männel D N, Orosz P, Hafner M, Falk W
Department of Pathology, University of Regensburg, Germany.
Circ Shock. 1994 Sep;44(1):9-13.
The enhancement of tumor metastasis by concurrent inflammatory processes is mainly due to the cytokines TNF and IL-1. In the case of TNF this effect is not restricted to metastasis models as measured by in vivo colony formation but also found in experimental model systems of spontaneous metastasis. Direct effects on the tumor cells or interference with the host NK cell system did not seem to account for the observed TNF effect. Experimental evidence from different test systems rather points to TNF- or IL-1-induced enhanced adhesion of tumor cells to the endothelial cell layer as the underlying mechanism. Blocking of integrin-matrix interactions with monoclonal antibodies or competing peptides inhibited tumor cell adhesion to endothelioma cells in vitro and lung colony formation of tumor cells in vivo.
同时发生的炎症过程对肿瘤转移的促进作用主要归因于细胞因子TNF和IL-1。就TNF而言，这种作用并不局限于通过体内集落形成来衡量的转移模型，在自发性转移的实验模型系统中也有发现。对肿瘤细胞的直接作用或对宿主自然杀伤细胞系统的干扰似乎并不能解释所观察到的TNF效应。来自不同测试系统的实验证据更倾向于认为，TNF或IL-1诱导肿瘤细胞与内皮细胞层的黏附增强是其潜在机制。用单克隆抗体或竞争性肽阻断整合素与基质的相互作用，可在体外抑制肿瘤细胞与内皮瘤细胞的黏附，并在体内抑制肿瘤细胞的肺集落形成。
