首页> 美国卫生研究院文献>Oncotarget >MicroRNA-92b inhibits epithelial-mesenchymal transition-induced migration and invasion by targeting Smad3 in nasopharyngeal cancer
【2h】

MicroRNA-92b inhibits epithelial-mesenchymal transition-induced migration and invasion by targeting Smad3 in nasopharyngeal cancer

机译:MicroRNA-92b通过靶向鼻咽癌中的Smad3抑制上皮-间质转化诱导的迁移和侵袭

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。
获取外文期刊封面目录资料

摘要

Increasing studies reports that aberrant miRNAs contribute to nasopharyngeal carcinoma (NPC) development and progression. However, the role of miR-92b in NPC remains unclear. In present research, we found that a reduced miR-92b expression in NPC tissues and cell lines. The clinical data showed that the down-regulated miR-92b expression was obviously associated with adverse prognostic characteristic. Furthermore, we confirmed that miR-92b was a novel independent prognostic symbol for predicting 5-year survival of NPC patients. MiR-92b overexpression inhibited cell migration, invasion and EMT progress, while down-regulated miR-92b reversed the effect. Besides, miR-92b could modulate Smad3 by directly binding to its 3’-UTR. In clinical samples of NPC, miR-92b inversely correlated with Smad3. Alternation of Smad3 expression at least partially abrogated the migration, invasion and EMT progress of miR-92b on NPC cells. In summary, our results indicated that miR-92b functioned as a tumor suppressor gene in regulating the EMT and metastasis of NPC via targeting Smad3, and may represent a novel potential therapeutic target and prognostic marker for NPC.
机译:越来越多的研究表明,异常的miRNA有助于鼻咽癌(NPC)的发展和进程。但是,尚不清楚miR-92b在NPC中的作用。在目前的研究中,我们发现在NPC组织和细胞系中miR-92b表达降低。临床数据表明,miR-92b表达下调明显与不良预后有关。此外,我们证实miR-92b是预测NPC患者5年生存的新型独立预后标志。 MiR-92b的过表达抑制细胞迁移,侵袭和EMT进程,而下调的miR-92b则逆转该作用。此外,miR-92b可以通过直接结合其3'-UTR来调节Smad3。在NPC的临床样本中,miR-92b与Smad3呈负相关。 Smad3表达的改变至少部分消除了miR-92b在NPC细胞上的迁移,侵袭和EMT进展。总之,我们的结果表明,miR-92b通过靶向Smad3在调节EMT和NPC转移中起着抑癌基因的作用,并且可能代表了NPC的新型潜在治疗靶点和预后标志物。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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