ArticleJournal of ovarian research2025
Trophoblast cell surface antigen 2 (TROP2) from ascitic extracellular vesicles drives peritoneal metastasis of ovarian cancer by mesothelial-to-mesenchymal transition.
Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Abstract
backgroundOvarian cancer (OvCA) exhibits a distinctive tendency toward peritoneal metastasis, a pathological process that greatly affects disease progression and postoperative recurrence. Understanding the biological mechanisms underlying this metastatic cascade is critical for improving prognosis and developing targeted therapeutic strategies. This study investigated the functional role of TROP2 in extracellular vesicles (EVs) from ovarian cancer ascites, and revealed how TROP2 induces mesothelial-mesenchymal transition (MMT) through EV-mediated intercellular communication. This process remodeled the mesothelial microenvironment into a pro-metastatic environment that enables peritoneal dissemination.
methodsEVs were isolated from ascites and cell culture supernatants through differential centrifugation combined with ultracentrifugation. After incubation with mesothelial cells, Western blot analysis, migration assays, and adhesion assays were performed to assess the induction of mesenchymal phenotype. Through proteomic profiling analysis of ascitic EVs, the differential protein TROP2 was identified and subsequently verificated clinical samples. TROP2 expression was modified through lentiviral transfection, and an orthotopic xenograft mouse model of ovarian cancer was established to evaluate tumor growth and metastasis through in vivo bioluminescence live imaging.
resultsEVs secreted by ovarian cancer cells induced phenotypic changes in mesenchymal cells and enhanced their adhesion to cancer cells. Proteomic analysis identified TROP2 as a differentially expressed protein in ascitic EVs. Phenotypic experiments indicated that EVs from ovarian cancer deliver TROP2 to peritoneal mesothelial cells, where it induces MMT and promotes peritoneal colonization in vitro. In the orthotopic mouse model of ovarian cancer, injection of TROP2-enriched EVs promoted peritoneal metastasis. Mechanistic investigations revealed that TROP2 induced the MMT process in mesothelial cells through activating the TNF-α/NF-κB pathway. Furthermore, treatment with quinazoline (QNZ), the TNF-α/NF-κB pathway inhibitor effectively reversed the TROP2 induced mesenchymal phenotype in mesothelial cells.
conclusionThis study is the first to identify the pivotal role of TROP2 from ascitic EV in promoting metastatic dissemination by activating the TNF-α/NF-κB signaling axis. By remodeling the peritoneal microenvironment, TROP2 facilitates metastatic spread. These findings provide novel molecular insights into the mechanism of ovarian cancer peritoneal metastasis and offer significant implications for clinical translation.
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