...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Endothelial-mesenchymal transition in normal human esophageal endothelial cells cocultured with esophageal adenocarcinoma cells: role of IL-1 beta and TGF-beta 2
【24h】

Endothelial-mesenchymal transition in normal human esophageal endothelial cells cocultured with esophageal adenocarcinoma cells: role of IL-1 beta and TGF-beta 2

机译：用食管腺癌细胞与食管腺癌细胞共同种植的正常人食管内皮细胞内皮 - 间充质转变：IL-1β和TGF-β的作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Endothelial-mesenchymal transition (EndoMT) has been recognized as a key determinant of tumor microenvironment in cancer progression and metastasis. Endothelial cells undergoing EndoMT lose their endothelial markers, acquire the mesenchymal phenotype, and become more invasive with increased migratory abilities. Early stages of esophageal adenocarcinoma (EAC) are characterized by strong mi-crovasculature whose impact in tumor progression remains undefined. Our aim was to determine the role of EndoMT in EAC by investigating the impact of tumor cells on normal primary human esophageal micro vascular endothelial cells (HEMEC). HEMEC were either cocultured with OE33 adenocarcinoma cells or treated with IL-lfS and transforming growth factor-p2 (TGF-fS2) for indicated periods and analyzed for EndoMT-associated changes by real-time PCR, Western blotting, immunofluorescence staining, and functional assays. Additionally, human EAC tissues were investigated for detection of EndoMT-like cells. Our results demonstrate an increased expression of mesenchymal markers [fibroblast-specific protein 1 (FSP1), collagenla2, vimentin, a-smooth muscle actin (a-SMA), and Snail], decreased expression of endothelial markers [CD31, von Willebrand factor VIII (vWF), and VE-cadherin], and elevated migration ability in HEMEC following coculture with OE33 cells. The EndoMT-related changes were inhibited by IL-1(3 and TGF-(32 gene silencing in OE33 cells. Recombinant IL-ip and TGF-(32 induced EndoMT in HEMEC. Although the level of VEGF expression was elevated in EndoMT cells, the angiogenic property of these cells was diminished. In vivo, by immunostaining EndoMT-like cells were detected at the invasive front of EAC. Our findings underscore a significant role for EndoMT in EAC and provide new insights into the mechanisms and significance of EndoMT in the context of tumor progression.
机译：内皮 - 间充质转换（endomt）被认为是癌症进展和转移中肿瘤微环境的关键决定因素。正在进行因子的内皮细胞失去其内皮标记物，获得间充质表型，并随着迁移能力增加而变得更加侵袭性。食管腺癌（EAC）的早期阶段的特征在于强大的Mi-Crocassulatureatoration，其对肿瘤进展的影响仍未确定。我们的目标是通过研究肿瘤细胞对正常的原发性人食管微血管内皮细胞（HEMEC）的影响来确定ENC在EAC中的作用。 Hemec与OE33腺癌细胞共同种质，或用IL-LFS处理并转化生长因子-P2（TGF-FS2）进行指定的时间，并通过实时PCR，Western印迹，免疫荧光染色和功能性测定分析为子宫内膜相关变化。另外，研究人的EAC组织以检测引起的细胞样细胞。我们的结果表明了间充质标记物的表达增加了[成纤维细胞特异性蛋白1（FSP1），Collagenla2，Vimentin，A-平滑肌肌动蛋白（A-SMA）和蜗牛]，降低内皮标记物的表达[CD31，von Willebrand因子VIII （VWF）和Ve-cadherin]，血统升高，升高了与OE33细胞的Hemec。 IL-1（33和OE33细胞中的32个基因沉默32个基因沉默）抑制了相关的变化。重组IL-IP和TGF-（32在Hemec中诱导的endomt。尽管VEGF表达的水平在引起的细胞中升高，这些细胞的血管生成性能降低。在体内，在EAC的侵袭性前面检测到免疫染色的子瘤细胞。我们的研究结果强调了EAC中因子的重要作用，并提供了对endomt的机制和意义的新洞察力肿瘤进展的背景。

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