ceRNA network construction and comparison of gastric cancer with or without Helicobacter pylori infection
ceRNA network construction and comparison of gastric cancer with or without Helicobacter pylori infection
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幽门螺杆菌感染与非幽门螺杆菌感染的胃癌ceRNA网络构建及比较
DOI：
10.1002/jcp.27467
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发表时间：
2019-05-01
影响因子：
5.6
通讯作者：
Wang, Yunshan
中科院分区：
文献类型：
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作者：
Liu, Yanyan;Zhu, Jingyu;Wang, Yunshan
胃癌（GC）是一种致死性疾病，其多种病因中，幽门螺杆菌（H. pylori）感染是最强的危险因素。然而，幽门螺杆菌相关GC的遗传和分子机制需要进一步阐明。我们研究了幽门螺杆菌 (+) 和幽门螺杆菌 (-) GC 之间竞争性内源 RNA (ceRNA) 网络差异。从 TCGA 数据库下载了 32 个相邻非癌样本以及 18 个幽门螺杆菌 (+) 和 141 个幽门螺杆菌 (-) 胃腺癌样本的长非编码 RNA (lncRNA)、microRNA (miRNA) 和信使 RNA (mRNA) 表达数据。构建幽门螺杆菌 (+) 和幽门螺杆菌 (-) GC 的 lncRNA-miRNA-mRNA ceRNA 网络后，使用 Panther 和 Kobas 数据库分析基因本体论 (GO) 和京都基因和基因组百科全书 (KEGG) 通路。最后，利用生存分析来发现关键基因。在幽门螺杆菌 (+) GC 中，我们总共鉴定了 1,419 个 lncRNA、82 个 miRNA 和 2,501 个具有差异表达谱的 mRNA。在幽门螺杆菌 (-) GC 中，2,225 个 lncRNA、130 个 miRNA 和 3,146 个 mRNA 差异表达。此外，幽门螺杆菌 (+) GC 中富集了三种独特的通路（细胞因子-细胞因子受体相互作用、HIF-1 信号通路和 Wnt 信号通路）。根据总体生存分析，三种 lncRNA（AP002478.1、LINC00111 和 LINC00313）和两种 mRNA（MYB 和 COL1A1）可作为幽门螺杆菌 (+) GC 患者的预后生物标志物。总之，我们的研究确定了幽门螺杆菌 (+) 和幽门螺杆菌 (-) GC 之间 ceRNA 调控网络的差异，并为未来的研究提供了丰富的候选库。
Gastric cancer (GC) is a lethal disease, and among its variety of etiological factors, Helicobacter pylori (H. pylori) infection is the strongest risk factor. However, the genetic and molecular mechanisms underlying H. pylori-related GC need further elucidation. We investigated the competing endogenous RNA (ceRNA) network differences between H. pylori (+) and H. pylori (-) GC. The long noncoding RNA (lncRNA), microRNA (miRNA), and messenger RNA (mRNA) expression data from 32 adjacent noncancerous samples and 18 H. pylori (+) and 141 H. pylori (-) stomach adenocarcinoma samples were downloaded from the TCGA database. After construction of lncRNA-miRNA-mRNA ceRNA networks of H. pylori (+) and H. pylori (-) GC, Panther and Kobas databases were used to analyze the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Finally, survival analysis was used to discover the key genes. In H. pylori (+) GC, we identified a total of 1,419 lncRNAs, 82 miRNAs, and 2,501 mRNAs with differentially expressed profiles. In H. pylori (-) GC, 2,225 lncRNAs, 130 miRNAs, and 3,146 mRNAs were differentially expressed. Furthermore, three unique pathways (cytokine-cytokine receptor interaction, HIF-1 signaling pathway, and Wnt signaling pathway) were enriched in H. pylori (+) GC. According to the overall survival analysis, three lncRNAs (AP002478.1, LINC00111, and LINC00313) and two mRNAs (MYB and COL1A1) functioned as prognostic biomarkers for patients with H. pylori (+) GC. In conclusion, our study has identified the differences in ceRNA regulatory networks between H. pylori (+) and H. pylori (-) GC and provides a rich candidate reservoir for future studies.