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首页> 外文期刊>Journal of experimental & clinical cancer research : >Hypoxic exosomes facilitate angiogenesis and metastasis in esophageal squamous cell carcinoma through altering the phenotype and transcriptome of endothelial cells
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Hypoxic exosomes facilitate angiogenesis and metastasis in esophageal squamous cell carcinoma through altering the phenotype and transcriptome of endothelial cells

机译：低氧外泌体通过改变内皮细胞的表型和转录组，促进食管鳞状细胞癌的血管生成和转移

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In cancer progression, hypoxia, or low oxygen tension, is a major regulator of tumor aggressiveness and metastasis. However, how cancer cells adapt to the hypoxia and communicate with other mesenchymal cells in microenvironment during tumor development remains to be elucidated. Here, we investigated the involvement of exosomes in modulating angiogenesis and enhancing metastasis in esophageal squamous cell carcinoma (ESCC). Differential centrifugation, transmission electron microscopy and nanoparticle tracking analysis were used to isolate and characterize exosomes. Colony formation and transwell assay were performed to assess the proliferation, migration and invasion of human umbilical vein endothelial cells (HUVECs). The tube formation assay and matrigel plug assay were used to evaluate the vascular formation ability of HUVECs in vitro and in vivo respectively. An in vivo nude mice model was established to detect the regulatory role of exosomes in ESCC progression. Microarray analysis was performed to analyze the transcriptome profiles in HUVECs. Exosomes derived from ESCC cells cultured under hypoxia played a better role in promoting proliferation, migration, invasion and tube formation of HUVECs in vitro and in vivo than exosomes from ESCC cells cultured under normoxia. Moreover, hypoxic exosomes significantly enhanced the tumor growth and lung metastasis compared with normoxic exosomes in nude mice models. Interestingly, endothelial cells were programmed by hypoxic and normoxic exosomes from ESCC cells which altered the transcriptome profile of HUVECs. Taken together, our data identified an angiogenic role of exosomes from ESCC cells which shed light on the further application of exosomes as valuable therapeutic target for ESCC.
机译：在癌症进展中，缺氧或低氧张力是肿瘤侵袭性和转移的主要调节剂。然而，在肿瘤发展过程中癌细胞如何适应缺氧并在微环境中与其他间充质细胞通讯仍需阐明。在这里，我们调查了外来体参与调节食管鳞状细胞癌（ESCC）的血管生成和增强转移​​。差速离心，透射电子显微镜和纳米粒子跟踪分析用于分离和表征外泌体。进行菌落形成和transwell测定以评估人脐静脉内皮细胞（HUVEC）的增殖，迁移和侵袭。分别用试管形成法和基质胶塞法评价HUVECs在体外和体内的血管形成能力。建立体内裸鼠模型以检测外泌体在ESCC进展中的调节作用。进行微阵列分析以分析HUVEC中的转录组谱。在低氧条件下培养的ESCC细胞衍生的外来体在体内外体内对HUVEC的增殖，迁移，侵袭和管形成的促进作用比在常氧条件下培养的ESCC细胞的外泌体更好。此外，与正常氧外泌体相比，低氧外泌体在裸鼠模型中显着增强了肿瘤的生长和肺转移。有趣的是，内皮细胞由来自ESCC细胞的低氧和常氧外来体编程，这改变了HUVEC的转录组谱。综上所述，我们的数据确定了来自ESCC细胞的外泌体的血管生成作用，这为进一步应用外泌体作为ESCC的有价值的治疗靶标提供了启示。

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