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Expression of Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 1 (SNHG1) Exacerbates Hepatocellular Carcinoma Through Suppressing miR-195

机译:长非编码RNA(lncRNA)小核仁RNA宿主基因1(SNHG1)的表达通过抑制miR-195加剧了肝细胞癌。

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BACKGROUND Aberrant expression of lncRNA has been suggested to have an association with tumorigenesis. Our study was designed to reveal the underlying connection between lncRNA SNHG1 and hepatocellular carcinoma (HCC) pathogenesis. MATERIAL AND METHODS A total of 122 pairs of HCC tissues (case group) and matched adjacent non-tumor liver tissues (control group) were collected for this study. RT-PCR and [i]in situ[/i] hybridization were conducted to investigate differences in lncRNA SNHG1 expression between the case and control group. The expression levels of lncRNA SNHG1 and miR-195 in HepG2 cells transfected with SNHG1-mimic and SNHG1-inhibitor were measured by RT-PCR. The proliferation, invasion, and migration status of HepG2 cells after transfection were assessed through MTT assay, wound healing assay, and Transwell assay, respectively. Whether miR-195 is a direct downstream target of lncRNA SNHG1 was verified by both bioinformatics target gene prediction and dual-luciferase report assay. RESULTS The expression level of lncRNA SNHG1 was remarkably upregulated in HCC tissues and cell lines compared with normal tissues and cell lines. High expression of lncRNA SNHG1 contributed to the downregulation of miR-195 in HepG2 cells. Also, lncRNA SNHG1 exacerbated HCC cell proliferation, invasion, and migration [i]in vitro[/i] through the inhibition of miR-195. This suggests that miR-195 is a direct downstream target of lncRNA SNHG1. CONCLUSIONS lncRNA SNHG1 may contribute to the aggravation of HCC through the inhibition of miR-195.
机译:背景技术已经表明lncRNA的异常表达与肿瘤发生有关。我们的研究旨在揭示lncRNA SNHG1与肝细胞癌(HCC)发病机理之间的潜在联系。材料与方法本研究共收集了122对HCC组织(病例组)和相匹配的相邻非肿瘤肝组织(对照组)。进行RT-PCR和[i]原位杂交以研究病例与对照组之间lncRNA SNHG1表达的差异。通过RT-PCR测定转染了SNHG1模拟物和SNHG1抑制剂的HepG2细胞中lncRNA SNHG1和miR-195的表达水平。转染后,分别通过MTT测定,伤口愈合测定和Transwell测定来评估HepG2细胞的增殖,侵袭和迁移状态。 miR-195是否是lncRNA SNHG1的直接下游靶标已通过生物信息学靶标基因预测和双荧光素酶报告检测法进行了验证。结果与正常组织和细胞株相比,肝癌组织和细胞株中lncRNA SNHG1的表达水平明显上调。 lncRNA SNHG1的高表达有助于HepG2细胞中miR-195的下调。而且,lncRNA SNHG1通过抑制miR-195在体外[/ i]加剧了HCC细胞的增殖,侵袭和迁移。这表明miR-195是lncRNA SNHG1的直接下游靶标。结论lncRNA SNHG1可能通过抑制miR-195而加剧了肝癌的发生。

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