Peritoneal metastasis (PM) is a very serious complication of gastrointestinal and gynecological malignancies which is poorly documented. Modified mesothelial cell layer and their microenvironments can favor fibrin deposition for cancer cell adhesion. Scanning and transmission electron microscopy of peritoneal surface and cancer cell clusters from cancer patients was done. Ascites and its impact on mesothelial cells were assessed by cytokine array. Neprilysin, matrix metalloprotease, epithelial mesenchymal transition (EMT) related molecules (E-cadherin, Snail, Slug, Twist, Vimentin and Fibronectin), tissues factor (TF), endothelial protein C receptors (EPCR) were quantified by q-PCR. Fibrin in the simples were stained using anti fibrin F1E1 antibody. Migration ability was assessed by scratch assay. Cell viability and neprilysin activity were analyzed by bioluminescence. Cancer cells-fibrin interaction was investigated by scanning electron microscopy (SEM) and microcinematography (MCG). Mesothelial cells change their morphology after incubation with carcinomatosis peritoneal fluids in vitro. EMT associated with upregulation of neprilysin, matrix metalloproteinase-2, tissue factor and cytokines secretions such as interleukin-6, and 8, hepatocyte growth factor and granulocyte chemotactic protein-2 mRNA and protein were observed. EPCR expression as a natural anticoagulant was decreased. In parallel, carcinomatosis cell clusters extracted from peritoneal fluids were found to be associated with fibrin. Kinetic analysis of cancer cell-fibrin interaction in vitro studied by MCG showed that fiber filaments generated from clots inhibited cancer cell adhesion on fibrin clots. These results indicated that fibrin deposit on the peritoneal surface serve as niches for cancer expansion in carcinomatosis patients.

中文翻译：

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腹膜表面的纤维蛋白沉积可作为癌变患者癌症扩展的利基市场。

腹膜转移（PM）是胃肠道和妇科恶性肿瘤的非常严重的并发症，文献报道很少。修饰的间皮细胞层及其微环境可促进纤维蛋白沉积，促进癌细胞粘附。进行了来自癌症患者的腹膜表面和癌细胞簇的扫描和透射电子显微镜检查。通过细胞因子阵列评估腹水及其对间皮细胞的影响。通过q-PCR定量测定了脑啡肽酶，基质金属蛋白酶，上皮间质转化（EMT）相关分子（E-钙粘着蛋白，蜗牛，Slug，Twist，波形蛋白和纤连蛋白），组织因子（TF），内皮蛋白C受体（EPCR）。使用抗纤维蛋白F1E1抗体对简单纤维蛋白进行染色。通过划痕测定评估迁移能力。通过生物发光分析细胞活力和中性溶酶活性。通过扫描电子显微镜（SEM）和微电影照相术（MCG）研究了癌细胞与纤维蛋白的相互作用。与癌变腹膜液一起孵育后，间皮细胞会改变其形态。观察到EMT与中性溶酶，基质金属蛋白酶-2，组织因子和细胞因子分泌如白细胞介素6和8的上调有关，肝细胞生长因子和粒细胞趋化蛋白-2 mRNA和蛋白。EPCR作为天然抗凝剂的表达下降。同时，发现从腹膜液中提取出的癌变细胞簇与纤维蛋白有关。MCG体外研究癌细胞-纤维蛋白相互作用的动力学分析表明，凝块产生的纤维丝抑制癌细胞粘附在纤维蛋白凝块上。这些结果表明，纤维蛋白沉积在腹膜表面上可作为癌变患者癌症扩展的利基。