细胞外囊泡（EV）是肿瘤微环境中癌细胞与其他类型细胞（例如肿瘤相关巨噬细胞（TAM））之间的介质。 EVs可以重塑肿瘤微环境并调节肿瘤进展。然而，这些相互作用的潜在分子机制仍不清楚。首先，我们探讨了TAMs对卵巢癌患者生存预后的影响。接下来，我们通过超速离心分离了源自卵巢癌细胞（OV-EV）的 EV，并分析了 OV-EV 调节卵巢肿瘤和全外周血中巨噬细胞极化的能力。此外，我们通过体外和体内测定探讨了OV-EVs诱导的巨噬细胞在肿瘤进展中的作用。OV-EVs被巨噬细胞包裹并诱导巨噬细胞向M2表型极化。此外，OV-EVs诱导的M2巨噬细胞在体外和体内均促进血管生成和癌症进展。此外，OV-EVs诱导的巨噬细胞增加了肿瘤中VEGF的表达水平和VEGFR的表达水平，从而导致卵巢癌中的血管生成。本研究表明OV-EVs诱导巨噬细胞中的M2极化并促进进展卵巢癌。这项研究为卵巢癌进展机制提供了新的见解。© 2024。作者。

Extracellular vesicles (EVs) are mediators between cancer cells and other types of cells, such as tumor-associated macrophages (TAMs), in the tumor microenvironment. EVs can remodel the tumor microenvironment and regulate tumor progression. However, the underlying molecular mechanism of these interactions remains unclear.First, we explored the effect of TAMs on the survival prognosis of patients with ovarian cancer. Next, we isolated EVs derived from ovarian cancer cells (OV-EVs) through ultracentrifugation and analyzed the capacity of OV-EVs to regulate macrophage polarization in ovarian tumors and in whole peripheral blood. Moreover, we explored the roles of OV-EVs-induced macrophages in tumor progression through in vitro and in vivo assays.OV-EVs were encapsulated by macrophages and induced the polarization of macrophages toward the M2 phenotype. Moreover, OV-EVs-induced M2 macrophages promoted angiogenesis and cancer progression both in vitro and in vivo. In addition, OV-EVs-induced macrophages increased the expression level of VEGF and increased the expression level of VEGFR in tumors, which resulted in angiogenesis in ovarian cancer.The present study demonstrated that OV-EVs induce M2 polarization in macrophages and promote the progression of ovarian cancer. This study provides novel insight into the mechanism of ovarian cancer progression.© 2024. The Author(s).