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首页> 外文期刊>Oncology letters >lncRNA FAM83H-AS1 is associated with the prognosis of colorectal carcinoma and promotes cell proliferation by targeting the Notch signaling pathway
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lncRNA FAM83H-AS1 is associated with the prognosis of colorectal carcinoma and promotes cell proliferation by targeting the Notch signaling pathway

机译:LNCRNA FAM83H-AS1与结肠直肠癌的预后相关,并通过靶向凹口信号通路来促进细胞增殖

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摘要

The long non-coding RNA, FAM83H antisense RNA 1 (head to head) (FAM83H-AS1), has exhibited a functional role as an oncogene in a number of different types of cancer. The aim of the present study was to reveal the dysregulation of FAM83H-AS1 in colorectal carcinoma (CRC) samples and elucidate its underlying associations with the Notch signaling pathway. The expression profiles of FAM83H-AS1 and two Notch signaling-associated molecules, Notch1 and Hes family basic-helix-loop-helix transcription factor 1 (Hes1), were measured by reverse transcription-polymerase chain reaction and western blot analysis. The Pearson chi(2) test was employed to evaluate the associations between FAM83H-AS1 expression and clinical features. A statistically significant positive association between the expression levels of FAM83H-AS1 and those of Notch1 or Hes1 in CRC tissues was analyzed by Spearman's correlation analysis. The Kaplan-Meier method was used to compare the overall survival curves between the highly-expressed and low-expressed FAM83H-AS1 groups via a log-rank test. Specific small hairpin RNA was transfected to silence endogenous FAM83H-AS1. MTT and colony formation assays were performed to measure the growth-inhibition effect of silenced FAM83H-AS1. The levels of FAM83H-AS1, Notch1 and Hes1 were significantly increased in CRC samples and cell lines. Cell proliferation was markedly inhibited when FAM83H-AS1 was knocked down and this effect mediated by FAM83H-AS1 could be reversed by Notch1 regulators. Thus, downregulated FAM83H-AS1 exhibited an anti-proliferative role in CRC by repressing the Notch signaling pathway.
机译:长期非编码RNA,FAM83H反义RNA 1(头部到头部)(FAM83H-AS1),在许多不同类型的癌症中表现出作为癌基因的功能作用。本研究的目的是揭示结直肠癌(CRC)样品中FAM83H-AS1的失调,并阐明其与NOTCH信号通路的潜在关联。通过逆转录 - 聚合酶链反应和Western印迹分析测量Fam83H-AS1和两种Notch信号相关分子,Notch1和HES系列碱性螺旋回路 - 螺旋转录因子1(HES1)的表达谱。 Pearson Chi(2)试验用于评估FAM83H-AS1表达和临床特征之间的关联。通过Spearman的相关性分析分析了FAM83H-AS1表达水平与CRC组织中NOTCH1或HES1之间的统计学显着的阳性关联。 KAPLAN-MEIER方法用于通过对数级测试进行比较高表达和低表达的FAM83-AS1组之间的整体生存曲线。将特定的小发夹RNA转染到沉默内源FAM83H-AS1。进行MTT和菌落形成测定以测量沉默的FAM83H-AS1的生长抑制作用。 FAM83H-AS1,NOTCH1和HES1的水平在CRC样品和细胞系中显着增加。当FAM83H-AS1被敲下来时,细胞增殖明显抑制,并且通过Notch1调节剂可以逆转FAM83H-AS1介导的这种效果。因此,下调的FAM83H-AS1通过压制缺口信号通路在CRC中表现出抗增殖性作用。

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