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首页> 外文期刊>Journal of Cellular Physiology >Horizontal transfer of miR‐23a from hypoxic tumor cell colonies can induce angiogenesis
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Horizontal transfer of miR‐23a from hypoxic tumor cell colonies can induce angiogenesis

机译:米尔的水平转移23从肿瘤缺氧细胞殖民地可以诱导血管生成

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Neo vessel formation by angiogenesis is an important event during many pathological conditions including cancer, where it is indispensable for tumor growth and survival. Although, various pro‐angiogenic cytokines and soluble factors, secreted by tumor cells, have been reported to promote angiogenesis, recent studies have shown regulatory role of exosomes, secreted by tumor cells in the process of angiogenesis. These exosomes are capable of carrying nucleic acids, proteins, etc., as their cargo. Under the light of these facts and considering the presence of miRNAs, the non‐coding RNAs capable of regulating target gene expression, as one of the major cargos in the exosomes, we investigated, whether exosomes derived from normoxic and hypoxic tumor cell colonies exhibit difference in levels of miR‐23~27~24 cluster members and if so, to check the significance of their horizontal transfer on the process of angiogenesis. Results of our study showed that exosomes secreted by hypoxic tumor cell colonies possess significantly higher levels of miR23a and can induce angiogenesis. Further, we have shown that exosomes secreted by cells that ectopically over express miR23a is capable of inducing angiogenesis in different angiogenic model systems such as CAM, in ovo Xenograft and HUVEC models systems. Further, mechanistic analysis revealed that miR23a driven regulation of angiogenesis is brought about by down regulation of SIRT1 in the recipient cells. Collectively, the results presented here suggest that exosomal transfer of miR23a from tumor cell colonies can induce the process of angiogenesis by targeting SIRT1 in the recipient endothelial cells.
机译:血管生成是一个新血管的形成重要的事件在许多病理条件包括癌症,它在哪里肿瘤的生长和生存不可或缺的。尽管如此,各种职业的血管生成细胞因子和溶性因素,由肿瘤细胞分泌的,据报道促进血管生成,最近研究表明监管液的作用,由肿瘤细胞分泌的过程中血管生成。核酸、蛋白质等,作为他们的货物。考虑microrna的存在,非编码rna应承担的调节目标基因的能力表达式,作为主要的货物之一液,我们调查是否液来自常氧和缺氧的肿瘤细胞殖民地表现出不同程度的米尔23 ~ 27 ~ 24集群成员和如果是,检查他们的水平转移的意义血管生成的过程。表明,液分泌肿瘤缺氧细胞殖民地拥有更高的水平miR23a和可以诱导血管生成。我们已经表明,液分泌细胞在表达ectopically miR23a能力在不同的血管生成的诱导血管生成模型系统,如凸轮、蛋和异种移植HUVEC模型系统。分析显示,miR23a驱动的监管血管生成是带来的监管SIRT1的受体细胞。总的来说,这里的结果提出建议exosomal miR23a从肿瘤细胞的转移殖民地可以诱导血管生成的过程通过瞄准SIRT1在收件人内皮细胞。

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