Tumour‐derived exosomes have been shown to induce pre‐metastatic niche formation, favoring metastatic colonization of tumour cells, but the underlying molecular mechanism is still not fully understood. In this study, we showed that exosomes derived from the LLC cells could indeed significantly enhance their intrapulmonary colonization. Circulating LLC‐derived exosomes were mainly engulfed by lung fibroblasts and led to the NF‐κB signalling activation. Further studies indicated that the exosomal miR‐3473b was responsible for that by hindering the NFKB inhibitor delta's (NFKBID) function. Blocking miR‐3473b could reverse the exosome‐mediated NF‐κB activation of fibroblasts and decrease intrapulmonary colonization of lung tumour cells. Together, this study demonstrated that the miR‐3473b in exosomes could mediate the interaction of lung tumour cells and local fibroblasts in metastatic sites and, therefore, enhance the metastasis of lung tumour cells.

中文翻译：

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肿瘤来源的外泌体miR-3473b通过激活局部成纤维细胞的核因子κB促进肺肿瘤细胞肺内定植。

肿瘤来源的外来体已被证明可诱导转移前的生态位形成，有利于肿瘤细胞的转移定植，但其潜在的分子机制仍未完全了解。在这项研究中，我们表明，来自LLC细胞的外泌体确实可以显着增强其肺内定植。循环LLC衍生的外来体主要被肺成纤维细胞吞噬，并导致NF-κB信号激活。进一步的研究表明，外泌体miR-3473b通过阻碍NFKB抑制剂δ（NFKBID）功能来对此负责。阻断miR-3473b可以逆转外来体介导的成纤维细胞NF-κB活化并减少肺肿瘤细胞的肺内定植。一起，