RP11-564D11.3 假基因表达的综合分析及其在肝细胞癌中的潜在作用。

Integrated analysis of pseudogene RP11-564D11.3 expression and its potential roles in hepatocellular carcinoma.

机构信息

The Key Laboratory of Endemic & Ethnic Diseases, Guizhou Medical University, Ministry of Education, Guiyang 550004, PR China.

The Key Laboratory of Medical Molecular Biology, Guizhou Medical University, Guizhou Province, Guiyang 550004, PR China.

出版信息

Epigenomics. 2019 Feb;11(3):267-280. doi: 10.2217/epi-2018-0152. Epub 2018 Oct 26.

DOI:10.2217/epi-2018-0152

PMID:30362374

Abstract

AIM

We aim to identify differentially expressed pseudogenes and investigate their functional roles in carcinogenesis.

MATERIALS & METHODS: Here, we identify dysregulated pseudogenes, analyze their prognostic values and investigate their potential functions through pseudogene-miRNA-mRNA network from public -omics repositories.

RESULTS

We identified 16 frequently upregulated pseudogenes among which high expression levels of RP11-564D11.3 was significantly associated with poor overall survival in seven types of human cancers. RP11-564D11.3 was strongly correlated with pathways in cancer, PI3K-Akt signaling pathway and the neurotrophin signaling pathway. Further studies revealed that RP11-564D11.3 functions as a competitive endogenous RNA through targeting VEGFA in hepatocellular carcinoma.

CONCLUSION

Our findings suggest RP11-564D11.3 as a novel biomarker and therapeutic potential target against hepatocellular carcinoma.

摘要

目的

我们旨在鉴定差异表达的假基因，并研究它们在肿瘤发生中的功能作用。

材料与方法

在这里，我们通过公共组学数据库中的假基因-miRNA-mRNA 网络，鉴定失调的假基因，分析它们的预后价值，并研究它们的潜在功能。

结果

我们鉴定出 16 个经常上调的假基因，其中 RP11-564D11.3 的高表达水平与七种人类癌症的总生存期不良显著相关。RP11-564D11.3 与癌症途径、PI3K-Akt 信号通路和神经生长因子信号通路强烈相关。进一步的研究表明，RP11-564D11.3 通过靶向肝细胞癌中的 VEGFA 作为竞争性内源性 RNA 发挥作用。