• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Up-Regulated Expression of miR-23a/b Targeted the Pro-Apoptotic Fas in Radiation-Induced thymic Lymphoma
【24h】

Up-Regulated Expression of miR-23a/b Targeted the Pro-Apoptotic Fas in Radiation-Induced thymic Lymphoma

机译：miR-23a / b的表达上调靶向放射诱导的胸腺淋巴瘤中的促凋亡Fas。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

biBackground /i/bMicroRNAs (miRNAs) are small, single-stranded, noncoding RNAs, which usually bind to the 3'-untranslated region of target mRNAs and are capable of inducing posttranscriptional gene regulation by blocking translation or by degrading the target mRNA. However, the expression level of miR-23 in radiation induced carcinogenesis is largely unknown. biMethods /i/bRadiation induced thymic lymphoma model in BALB/c mice was set up. miR-23a & miR-23b miRNA levels in different tissues and cells were detected by real-time qPCR. miR-23a/b inhibitor and miR-23a/b mimics were transfected to lymphoma cells and the target of miR-23a/b was identified by microRNA target prediction and Luciferase assays. biResults /i/bWe found that miR-23a & miR-23b were up-regulated in radiation induced thymic lymphoma tissue samples. Cell death and apoptosis were increased by miR-23a/b inhibitor and decreased by miR-23a/b mimics in lymphoma cells. Computational analysis found a putative target site of miR-23a/b in the 3′UTR of Fas mRNA, which was verified by luciferase reporter assay. Forced over-expression of miR-23a/b decreased the level of Fas protein. Moreover, over-expression of Fas rescued the pro-proliferation effect of miR-23, indicating Fas is a direct mediator of miR-23 functions. Furthermore, contrast to miR-23a/b which was up regulated, the Fas expression level was down-regulated and inversely correlated with miR-23 in split radiation induced lymphoma tissue samples. Finally, our data also indicates that miR-23a could repress Fas much more potent than miR-23b and the additional region besides conserved seed pairing enables miR-23a's higher regulation. biConclusions /i/bIn this study, using a radiation induced thymic lymphoma model in BALB/c mice, We conclude that the expression of miR-23a/b is up-regulated in radiation-induced thymic lymphoma and it maybe a novel therapeutic target of that cancer.
机译：背景 MicroRNA（miRNA）是小的单链非编码RNA，通常与目标mRNA的3'-非翻译区结合，并能够诱导转录后基因调控通过阻断翻译或降解靶mRNA。但是，miR-23在辐射诱导的癌变过程中的表达水平尚不清楚。 方法 建立了BALB / c小鼠辐射诱发的胸腺淋巴瘤模型。 miR-23a＆＃38;通过实时qPCR检测不同组织和细胞中的miR-23b miRNA水平。将miR-23a / b抑制剂和miR-23a / b模拟物转染到淋巴瘤细胞，并通过microRNA靶标预测和荧光素酶测定法鉴定miR-23a / b的靶标。 结果 我们发现miR-23a＆＃38;在辐射诱导的胸腺淋巴瘤组织样品中，miR-23b上调。 miR-23a / b抑制剂可增加细胞死亡和凋亡，miR-23a / b模仿物可降低淋巴瘤细胞的死亡和凋亡。计算分析在Fas mRNA的3'UTR中发现了一个miR-23a / b的靶位点，这已通过荧光素酶报告基因检测得到了证实。强迫过度表达miR-23a / b降低了Fas蛋白的水平。此外，Fas的过度表达挽救了miR-23的增殖作用，表明Fas是miR-23功能的直接介体。此外，与上调的miR-23a / b相反，Fas表达水平下调并且在分裂放射诱导的淋巴瘤组织样品中与miR-23呈负相关。最后，我们的数据还表明，miR-23a抑制Fas的能力比miR-23b强得多，除保守的种子配对外，其他区域还可以抑制miR-23a的更高调控。 结论 在这项研究中，使用辐射诱导的BALB / c小鼠胸腺淋巴瘤模型，我们得出结论认为miR-23a / b的表达在辐射-引起的胸腺淋巴瘤，可能是该癌症的新治疗靶点。

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