Leroy-Dudal Johanne, Heyman Loraine, Gauduchon Pascal, Carreiras Franck
ERRMECe, EA 1391, UFR Sciences et Techniques, 2 rue Adolphe Chauvin, 95302 Cergy-Pontoise Cedex, France.
Cell Biol Int. 2005 Jun;29(6):482-8. doi: 10.1016/j.cellbi.2005.01.008.
Several lines of evidence suggest that vascularization plays an important role in the growth, local expansion and dissemination of ovarian epithelial tumours. However, the interaction of ovarian carcinoma cells with the endothelium remains poorly understood. To investigate adhesive events underlying this process, we used an in vitro model of cocultures between the IGROV1 human ovarian adenocarcinoma cell line and human umbilical vein endothelial cells (HUVECs). IGROV1 cells were shown to adhere rapidly on the HUVECs monolayer. Adhesion was inhibited by anti-alphav integrin and anti-Vn blocking antibodies, but not by anti-beta1 integrin antibodies. Anchorage of carcinoma cells led to the rupture of endothelial integrity, as revealed by the formation of holes in the monolayer and by the disappearance of the interendothelial VE-Cadherin network. Considering the ability of ovarian carcinoma to disseminate by a haematogenous way, these in vitro events could mimic a preliminary step for carcinoma cells crossing the endothelial barrier to extravasate.
多项证据表明,血管生成在卵巢上皮肿瘤的生长、局部扩展和播散中起重要作用。然而,卵巢癌细胞与内皮细胞之间的相互作用仍知之甚少。为了研究这一过程背后的黏附事件,我们使用了IGROV1人卵巢腺癌细胞系与人类脐静脉内皮细胞(HUVECs)共培养的体外模型。结果显示,IGROV1细胞能迅速黏附于HUVECs单层细胞上。抗αv整合素和抗Vn阻断抗体可抑制黏附,但抗β1整合素抗体则无此作用。癌细胞的黏附导致内皮完整性破坏,表现为单层细胞上出现孔洞以及内皮细胞间VE-钙黏蛋白网络消失。鉴于卵巢癌有通过血行途径播散的能力,这些体外事件可能模拟了癌细胞穿越内皮屏障以渗出的初步步骤。