...
首页> 外文期刊>International journal of biological sciences >Extracellular Vesicles (EVs) from Lung Adenocarcinoma Cells Promote Human Umbilical Vein Endothelial Cell (HUVEC) Angiogenesis through Yes Kinase-associated Protein (YAP) Transport
【24h】

Extracellular Vesicles (EVs) from Lung Adenocarcinoma Cells Promote Human Umbilical Vein Endothelial Cell (HUVEC) Angiogenesis through Yes Kinase-associated Protein (YAP) Transport

机译:来自肺腺癌细胞的细胞外囊泡(EVS)通过是激酶相关蛋白(YAP)运输促进人脐静脉内皮细胞(HUVEC)血管生成

获取原文
   

获取外文期刊封面封底 >>

       

摘要

Yes kinase-associated protein (YAP) plays an important role in angiogenesis and can promote the occurrence and development of many tumor types. However, whether YAP affects tumor angiogenesis in lung cancer, and its potential mechanism in lung cancer, are unknown. In this study, we explored the role of YAP in the angiogenesis of lung adenocarcinoma, and further illustrated its possible mechanism. The expression levels of YAP and the vascular endothelial marker protein CD31 were examined by immunohistochemistry and immunofluorescence in human lung adenocarcinoma tissues, revealing a possible positive correlation between YAP and CD31 in lung adenocarcinoma. The results of the western blotting (WB) of Human Umbilical Vein Endothelial Cells (HUVECs) after coculture with lung adenocarcinoma H1975 cells, H1975 cell-supernatants and H1975-derived EVs showed that YAP derived from H1975 cells can enter HUVECs via EVs. These results were confirmed by immunofluorescence. Finally, we generated H1975 low-YAP expression cells by transfecting the cells with a shYAP lentivirus, and confirmed that the low expression of YAP in H1975 cells inhibits HUVEC angiogenesis by reducing the amount of YAP that enters HUVECs. We found, for the first time, that YAP promotes angiogenesis in lung adenocarcinoma via EVs, at least partially. Our work may provide a promising method for lung cancer treatment by targeting angiogenesis in the future.? The author(s).
机译:是激酶相关蛋白(YAP)在血管生成中起重要作用,可以促进许多肿瘤类型的发生和发展。然而,yap是否影响肺癌中的肿瘤血管生成,其肺癌中的潜在机制是未知的。在这项研究中,我们探讨了YAP在肺腺癌的血管生成中的作用,并进一步说明了其可能的机制。通过免疫组织化学和人肺腺癌组织中的免疫组化和免疫荧光检查YAP和血管内皮标记蛋白CD31的表达水平,揭示了肺腺癌中的YAP和CD31之间的阳性相关性。人脐静脉内皮细胞(HUVECS)的蛋白质印迹(WB)的结果与肺腺癌H1975细胞,H1975细胞上清液和H1975衍生的EV显示出来,来自H1975细胞的YAP可以通过EVS进入HUVECS。这些结果通过免疫荧光证实。最后,我们通过用Shyap Lentivirus转染细胞来产生H1975低yap表达细胞,并证实了H1975细胞中YAP的低表达通过减少进入HUVECS的YAP的量来抑制HUVEC血管生成。我们首次发现Yap通过EVS,至少部分地促进肺腺癌血管生成。我们的作品可以通过将来靶向血管生成来提供肺癌治疗的有希望的方法。作者。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号