...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Signalling >Epigenetic repression of miR-132 expression by the hepatitis B virus x protein in hepatitis B virus-related hepatocellular carcinoma
【24h】

Epigenetic repression of miR-132 expression by the hepatitis B virus x protein in hepatitis B virus-related hepatocellular carcinoma

机译：乙型肝炎病毒相关肝细胞癌中乙型肝炎病毒x蛋白对miR-132表达的表观遗传抑制

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

Hepatitis B virus x (HBx) protein is involved in the initiation and progression of HBV-related hepatocellular carcinoma (HCC) by regulating host protein-coding genes. However, the role of HBx in the epigenetic repression of miRNAs, which play important roles in gene regulation during hepatocarcinogenesis, remains largely unknown. In this study, the expression of miR-132 in HCC cells, HBV-related HCC tissues, and serum were determined using real-time PCR. The level of DNA methylation on the promoter of miR-132 was examined using methylation-specific PCR (MSP). MiR-132 was functionally characterized in HCC cells with transiently altered miR-132 expression. HBx-induced DNA hypermethylation of the promoter of miR-132 was found to be more prevalent in HBx-expressing HepG2 cells than in control cells. Consistently, MiR-132 expression was also more frequently down-regulated in HBV-related HCC tissues than in adjacent noncancerous hepatic tissues and had a significant inverse correlation with HBx expression in HBV-related HCCs. Serum miR-132 levels were found to be significantly correlated with levels in tumor tissue. Finally, proliferation and colony formation of HCC cells were found to be suppressed by miR-132-mediated inhibition of the Akt-signaling pathway in miR132 transfected cells. Our study has demonstrated the epigenetic repression of miR-132 expression through DNA methylation induced by HBx. This work provides novel mechanistic insights into HBV-mediated hepatocarcinogenesis and suggests that miR-132 may be a promising biochemical marker and may have therapeutic applications in HBV-related HCC.
机译：乙型肝炎病毒x（HBx）蛋白通过调节宿主蛋白编码基因，参与HBV相关肝细胞癌（HCC）的发生和发展。然而，HBx在miRNA的表观遗传抑制中的作用，在肝癌发生过程中的基因调控中起着重要的作用，目前仍是未知之数。在这项研究中，使用实时荧光定量PCR检测miR-132在HCC细胞，HBV相关HCC组织和血清中的表达。使用甲基化特异性PCR（MSP）检测了miR-132启动子上的DNA甲基化水平。在具有短暂改变的miR-132表达的HCC细胞中对MiR-132进行了功能表征。发现在表达HBx的HepG2细胞中，HBx诱导的miR-132启动子的DNA甲基化程度高于对照细胞。一致地，与相邻的非癌性肝组织相比，在HBV相关的HCC组织中MiR-132的表达也更频繁地下调，并且与HBV相关的HCC中的HBx表达负相关。发现血清miR-132水平与肿瘤组织中的水平显着相关。最后，发现miC-132介导的miR132转染细胞中Akt信号通路的抑制可抑制HCC细胞的增殖和集落形成。我们的研究表明，通过HBx诱导的DNA甲基化，miR-132表达的表观遗传抑制。这项工作提供了有关HBV介导的肝癌发生的新机制的见解，并表明miR-132可能是有前途的生化标志物，并且可能在HBV相关HCC中具有治疗应用。

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