首页> 美国卫生研究院文献>Cancer Medicine >LncRNA SNHG3 sponges miR‐577 to up‐regulate SMURF1 expression in prostate cancer
【2h】

LncRNA SNHG3 sponges miR‐577 to up‐regulate SMURF1 expression in prostate cancer

机译:LncRNA SNHG3使miR‐577上调前列腺癌中SMURF1的表达

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。

摘要

Prostate cancer remains one of the most prevalent cancers and the main causes of cancer‐related deaths in males. Various articles introduced that long noncoding RNAs (lncRNAs) are found in vital functions in the development and progression of cancers. Although SNHG3 (small nucleolar RNA host gene 3) has been investigated in many cancers, now researches on the role and mechanism of SNHG3 in prostate cancer are lacked. In this work, SNHG3 exerted high expression in prostate cancer cell lines. Suppression of SNHG3 inhibited cell proliferation, migration, EMT (epithelial‐mesenchymal transition) process and promoted cell apoptosis. Additionally, it was found that SNHG3 could bind with miR‐577. Subsequently, SMURF1 (Smad ubiquitination regulatory factor 1) was identified as a downstream target of miR‐577 and had a negative correlation with miR‐577. SNHG3 was found to positively regulate SMURF1 expression. Furthermore, rescue assays demonstrated that co‐transfection of pcDNA3.1/SMURF1 reversed the effects of SNHG3 knockdown in cell proliferation, migration, EMT process and cell apoptosis. SNHG3 also promoted tumorigenesis in vivo. All the results above explained that SNHG3 accelerated prostate cancer progression by sponging miR‐577 to up‐regulate SMURF1 expression, suggesting that SNHG3 may act as a biomarker for prostate cancer patients.
机译:前列腺癌仍然是最普遍的癌症之一,也是男性与癌症相关的死亡的主要原因。各种文章介绍了长非编码RNA(lncRNA)被发现在癌症的发展和进程中的重要功能。尽管已经在许多癌症中研究了SNHG3(小核仁RNA宿主基因3),但是目前尚缺乏关于SNHG3在前列腺癌中的作用和机制的研究。在这项工作中,SNHG3在前列腺癌细胞系中发挥高表达。 SNHG3的抑制抑制细胞增殖,迁移,EMT(上皮-间质转化)过程并促进细胞凋亡。此外,还发现SNHG3可以与miR-577结合。随后,SMURF1(Smad泛素调节因子1)被确定为miR-577的下游靶标,并且与miR-577呈负相关。 SNHG3被发现正调控SMURF1表达。此外,急救分析表明,pcDNA3.1 / SMURF1的共转染逆转了SNHG3敲低对细胞增殖,迁移,EMT过程和细胞凋亡的影响。 SNHG3还促进体内肿瘤发生。以上所有结果均说明,SNHG3通过使miR-577海绵化以上调SMURF1表达而加速了前列腺癌的进展,表明SNHG3可能充当前列腺癌患者的生物标志物。

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