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首页> 外文期刊>Nature cancer. >Melanoma-derived small extracellular vesicles induce lymphangiogenesis and metastasis through an NGFR-dependent mechanism
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Melanoma-derived small extracellular vesicles induce lymphangiogenesis and metastasis through an NGFR-dependent mechanism

机译：Melanoma-derived小细胞外囊泡诱导lymphangiogenesis和转移一个NGFR-dependent机制

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摘要

Secreted extracellular vesicles (EVs) influence the tumor microenvironment and promote distal metastasis. Here we analyzed the involvement of melanoma-secreted EVs in lymph node pre-metastatic niche formation in murine models. We found that small EVs (sEVs) derived from metastatic melanoma cell lines were enriched in nerve growth factor (NGF) receptor (NGFR, p75NTR), spread through the lymphatic system and were taken up by lymphatic endothelial cells, reinforcing lymph node metastasis. Remarkably, sEVs enhanced lymphangiogenesis and tumor cell adhesion by inducing ERK kinase, nuclear factor (NF)-kB activation and intracellular adhesion molecule (ICAM)-1 expression in lymphatic endothelial cells. Importantly, ablation or inhibition of NGFR in sEVs reversed the lymphangiogenic phenotype, decreased lymph node metastasis and extended survival in pre-clinical models. Furthermore, NGFR expression was augmented in human lymph node metastases relative to that in matched primary tumors, and the frequency of NGFR+ metastatic melanoma cells in lymph nodes correlated with patient survival. In summary, we found that NGFR is secreted in melanoma-derived sEVs, reinforcing lymph node pre-metastatic niche formation and metastasis.
机译：分泌细胞外囊泡(EVs)的影响肿瘤微环境,促进远端转移。melanoma-secreted EVs淋巴结pre-metastatic利基在小鼠模型中形成。我们发现小电动车(股票)来自转移性黑素瘤细胞系是丰富的神经生长因子神经生长因子受体(NGFR,p75NTR),通过淋巴系统和传播是由淋巴内皮细胞,加强淋巴结转移。塞夫增强lymphangiogenesis和肿瘤细胞附着力诱导ERK激酶,核因子(NF) kb活化和细胞内的附着力分子(ICAM) 1表达的淋巴内皮细胞。抑制NGFR塞扭转了lymphangiogenic表型,减少淋巴结转移和延长生存在临床前模型。增强人类淋巴结转移相关在匹配的原发性肿瘤,NGFR +转移性黑色素瘤细胞的频率淋巴结与患者的生存。总结,我们发现NGFR分泌melanoma-derived塞,加强淋巴结pre-metastatic利基形成和转移。

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