缺氧肿瘤源性外泌体miR-1225-5p通过toll样受体2调节M2巨噬细胞极化,促进卵巢癌进展。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2023-12-01 Epub Date: 2023-11-27 DOI:10.1080/08916934.2023.2281226
Shu Tan, Hao Yu, Zhaocong Zhang, Yiming Liu, Ge Lou
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引用次数: 0

摘要

肿瘤分泌外泌体对肿瘤相关巨噬细胞(tam)的功能调节至关重要。本研究旨在探讨卵巢癌细胞分泌的外泌体如何调节巨噬细胞的表型和功能。假设缺氧处理A2780细胞模拟肿瘤微环境,外泌体与tam共培养。miR-1225-5p在缺氧外泌体中富集,并通过调节toll样受体2表达(TLR2)促进M2巨噬细胞极化。此外,缺氧处理的巨噬细胞通过wnt/β-catenin途径促进卵巢癌细胞的活力、迁移和侵袭。本研究阐明外泌体miR-1225-5p通过靶向TLR2促进卵巢癌发生,从而促进巨噬细胞m2样极化,可能通过wnt/β-catenin途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypoxic tumour-derived exosomal miR-1225-5p regulates M2 macrophage polarisation via toll-like receptor 2 to promote ovarian cancer progress.

Tumor-secreted exosomes are critical for the functional regulation of tumor-associated macrophages (TAMs). This study aimed to explore how exosomes secreted by ovarian carcinoma cells regulate the phenotype and function of macrophages. Hypoxic treatment of A2780 cells was postulated to mimic the tumor microenvironment, and exosomes were co-cultured with TAMs. miR-1225-5p was enriched in hypoxic exosomes and contributed to M2 macrophage polarizationby modulating Toll-like receptor 2 expression (TLR2). Furthermore, hypoxia-treated macrophages promote ovarian cancer cell viability, migration, and invasion via the wnt/β-catenin pathway. This study clarified that exosomal miR-1225-5p promotes macrophage M2-like polarization by targeting TLR2 to promote ovarian cancer, which may via the wnt/β-catenin pathway.

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CiteScore
7.20
自引率
4.30%
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