...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of cellular biochemistry. >Overexpression of Long Non‐Coding RNA MEG3 Inhibits Proliferation of Hepatocellular Carcinoma Huh7 Cells via Negative Modulation of miRNA‐664
【24h】

Overexpression of Long Non‐Coding RNA MEG3 Inhibits Proliferation of Hepatocellular Carcinoma Huh7 Cells via Negative Modulation of miRNA‐664

机译：长期非编码RNA Meg3的过度表达通过MiRNA-664的阴性调节抑制肝细胞癌HUH7细胞的增殖

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

ABSTRACT Evidence is accumulating that long non‐coding RNAs (lncRNAs) are involved in human tumorigenesis and dysregulated in many cancers, including hepatocellular carcinoma (HCC). Because lncRNAs can regulate essential pathways that contribute to tumor initiation and progression with their tissue specificity, lncRNAs are valuable biomarkers and therapeutic targets. Maternally expressed gene 3 (MEG3) is a lncRNA overexpressed in HCC cells that inhibits HCC progression, however, the mechanism remains largely unknown. Recently, a novel regulatory mechanism has been proposed in which RNAs can cross‐talk with each other via competing for shared microRNAs (miRNAs). The proposed competitive endogenous RNAs could mediate the bioavailability of miRNAs on their targets, thus imposing another level of post‐transcriptional regulation. In the current study, we demonstrated that MEG3 is down‐regulated in HCC tissues. MEG3 over‐expression imposes another level of post‐transcriptional regulation, whereas MEG3 overexpression increase the expression of the miR‐664 target gene, ADH4, through competitive “sponging” miR‐664. In addition, NF‐κB may affect transcription of MEG3 by directly binding to the promoter region. Our data revealed that NF‐κB may affect the transcript of MEG3. MEG3 overexpression inhibited the proliferation of HCC cells, at least in part by affecting miR‐664mediated regulation of ADH4. Together, these results suggest that MEG3 is a suppressor of tumor which acts in part through “sponging” miR‐664. J. Cell. Biochem. 118: 3713–3721, 2017. ? 2017 Wiley Periodicals, Inc.
机译：摘要证据积累了长期非编码RNA（LNCRNA）参与人类肿瘤内酯和在许多癌症中的失调，包括肝细胞癌（HCC）。因为LNCRNA可以调节有助于肿瘤起始和随着组织特异性的进展的基本途径，因此LNCRNA是有价值的生物标志物和治疗靶标。母体表达的基因3（MEG3）是在HCC细胞中过表达的LNCRNA，但抑制HCC进展，然而，该机制仍然很大程度上是未知的。最近，已经提出了一种新的监管机制，其中RNA可以通过竞争共享的MicroRNAS（MiRNA）互相交流。所提出的竞争内源性RNA可以介导MIRNA对其目标的生物利用度，从而施加另一个水平的转录后调节。在目前的研究中，我们证明MEG3在HCC组织中受到了下调。 MEG3过表达施加另一水平的转录后调节，而MEG3过表达通过竞争性“海绵”MIR-664增加了MIR-664靶基因ADH4的表达。此外，NF-κB可以通过直接与启动子区直接结合来影响MEG3的转录。我们的数据显示，NF-κB可能会影响MEG3的转录物。 MEG3过表达至少部分地通过影响ADH4的miR-664介导的调节来抑制HCC细胞的增殖。这些结果表明MEG3是肿瘤的抑制器，其部分通过“海绵”miR-664作用。 J.Cell。生物学习。 118：3713-3721,2017。？ 2017年Wiley期刊，Inc。

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