由于转移率高，胰腺癌（PC）是最具侵袭性的恶性肿瘤之一。需要阐明转移的机制。小细胞外囊泡 (sEV) 介导细胞间通讯，而癌症衍生的 sEV 有助于转移前生态位的形成。本研究检查了PC来源的sEV内化至血管内皮细胞中引起的粘附性变化，并研究了转移的分子机制。将胰腺癌来源的sEV内化至血管内皮细胞中，并评估了粘附性的变化。我们评估了 sEV 对体内肝转移形成的影响。我们还评估了 PC 衍生的 sEV 内化引起的血管内皮细胞的分子变化。PC 衍生的 sEV 内化到血管内皮细胞中促进了血管内皮细胞和 PC 细胞的粘附。胰腺癌衍生的 sEV 含有高水平的转化生长因子 β1 mRNA，并充当其转运蛋白。一旦PC源性sEVs内化到血管内皮细胞中，细胞表面纤连蛋白1的表达增加，血管内皮细胞的粘附性增强。我们研究了PC源性sEVs与粘附性之间的关系。 PC 衍生的 sEV 的调节具有作为抑制 PC 转移的治疗方式的潜力。版权所有 © 2024 Wolters Kluwer Health, Inc. 保留所有权利。

Pancreatic cancer (PC) is one of the most aggressive malignancies due to the high rate of metastasis. The mechanisms underlying metastasis need to be elucidated. Small extracellular vesicles (sEVs) mediate cell-to-cell communication, and cancer-derived sEVs contribute to the formation of premetastatic niches. The present study examined changes in adhesiveness by the internalization of PC-derived sEVs into vascular endothelial cells, and investigated the molecular mechanisms underlying metastasis.Pancreatic cancer-derived sEVs were internalized into vascular endothelial cells, and changes in adhesiveness were evaluated. We evaluated the effects of sEVs on the formation of liver metastasis in vivo. We also assessed molecular changes in vascular endothelial cells by the internalization of PC-derived sEVs.The internalization of PC-derived sEVs into vascular endothelial cells promoted the adhesiveness of vascular endothelial cells and PC cells. Pancreatic cancer-derived sEVs contained high levels of transforming growth factor β1 mRNA and acted as its transporter. Once PC-derived sEVs were internalized into vascular endothelial cells, the expression of fibronectin 1 increased on the cell surface, and the adhesiveness of vascular endothelial cells was enhanced.We investigated association between PC-derived sEVs and adhesiveness. Regulation of PC-derived sEVs has potential as a therapeutic modality to suppress the metastasis of PC.Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.