Up-regulation of LncRNA SNHG20 Predicts Poor Prognosis in Hepatocellular Carcinoma.

Up-regulation of LncRNA SNHG20 Predicts Poor Prognosis in Hepatocellular Carcinoma.
复制标题

LncRNA SNHG20 的上调预示着肝细胞癌的不良预后

DOI:
10.7150/jca.13822
复制
发表时间:
2016
期刊:
影响因子:
3.9
通讯作者:
Wu D
Wu D
中科院分区:
医学3区
文献类型:
--
作者:
Zhang D;Cao C;Liu L;Wu D

文献摘要

被引文献

相似文献

最近的研究表明,长链非编码RNA(lncRNA)在肿瘤的发生和发展中起着重要的调控作用。然而,小核仁RNA宿主基因20(SNHG 20)对癌症发展的贡献在很大程度上仍然未知。本研究旨在探讨SNHG 20在肝细胞癌(HCC)中的表达及其临床意义。我们的结果显示,SNHG 20的表达显着上调,与相邻的非肿瘤肝组织49例新鲜肝癌样本(队列1)通过定量逆转录聚合酶链反应(qRT-PCR,P = 0.004)检测。通过原位杂交(ISH)在144例福尔马林固定、石蜡包埋的HCC组织(队列2)中证实了该结果。SNHG 20的表达与肿瘤大小(队列1 P = 0.027,队列2 P = 0.046)和临床分期(队列1 P = 0.027,队列2 P = 0.028)相关。重要的是,SNHG 20高表达患者的总生存期(OS,P < 0.001)和无病生存期(DFS,P < 0.001)比SNHG 20低表达患者短。单因素和多因素分析显示SNHG 20是影响肝癌患者生存期的独立危险因素(危险比= 3.985,95% CI = 1.981-8.017,P < 0.001)。此外,来自癌症基因组图谱项目(TCGA)的总共331名HCC患者的数据被用来验证我们的发现。TCGA HCC队列研究结果显示SNHG 20在HCC组织中的表达明显高于非肿瘤肝组织(P < 0.001)。SNHG 20表达水平越高,患者的OS(P = 0.021)和DFS(P < 0.001)越差。在功能上,SK-Hep-1细胞中SNHG 20的敲低显著抑制细胞增殖、迁移和侵袭。总之,SNHG 20在HCC患者中表达上调,可作为HCC患者独立的预后预测因子。
Recent studies indicated that long noncoding RNAs (lncRNAs) played important regulatory roles in carcinogenesis and cancer progression. However, the contribution of small nucleolar RNA host gene 20 (SNHG20) to cancer development remains largely unknown. The aim of the study is to investigate the expression of SNHG20 and its clinical significance in hepatocellular carcinoma (HCC). Our results showed that the expression of SNHG20 was remarkably up-regulated in HCC tissues compared with adjacent non-tumor liver tissues from 49 fresh HCC samples (cohort 1) detected by quantitative reverse-transcription polymerase chain reaction (qRT-PCR, P = 0.004). The results were confirmed in 144 formalin-fixed, paraffin-embedded HCC tissues (cohort 2) by in situ hybridization (ISH). Meanwhile, the expression of SNHG20 was associated with tumor size (P = 0.027 for cohort 1 and P = 0.046 for cohort 2) and clinical stage (P = 0.027 for cohort 1 and P = 0.028 for cohort 2). Importantly, patients with high expression of SNHG20 had a shorter overall survival (OS, P < 0.001) and disease-free survival (DFS, P < 0.001) than those with low expression of SNHG20. Univatiate and multivariate analysis showed that SNHG20 was a significant and independent prognostic predictor for OS of HCC patients (hazard ratio = 3.985, 95% CI = 1.981-8.017, P < 0.001). In addition, a total of 331 HCC patients' data from the Caner Genome Atlas project (TCGA) were used to validate our findings. Consistently, the results from TCGA HCC cohort demonstrated that SNHG20 were overexpressed in HCC tissues compared with non-tumor liver tissues (P < 0.001). Patients with higher expression levels of SNHG20 had poorer OS (P = 0.021) and DFS (P < 0.001). Functionally, knockdown of SNHG20 in SK-Hep-1 cells significantly inhibited cellular proliferation, migration, and invasion. In conclusion, SNHG20, up-regulated in patients with HCC, may serve as an independent prognostic predictor for HCC patients.