Abstract
BackgroundDysregulated expression of long non-coding RNAs (lncRNAs) has been reported in the pathogenesis and progression of multiple cancers, including hepatocellular carcinoma (HCC). LncRNA CTD-2547G23.4 is a novel lncRNA, and its role in HCC is still unknown. Here, we aimed to clarify the expression pattern and clinical value of CTD-2547G23.4 and to investigate the prospective regulatory mechanism via bioinformatics analysis in HCC.MethodsTo identify differentially expressed lncRNAs in HCC, we downloaded RNA-Seq data for HCC and adjacent non-tumour tissues via The Cancer Genome Atlas (TCGA). CTD-2547G23.4 was selected by using the R language and receiver operating characteristic curve analysis. Furthermore, we validated the differential expression of CTD-2547G23.4 via Gene Expression Omnibus (GEO), ArrayExpress, Oncomine databases and quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between the CTD-2547G23.4 level and clinic pathological parameters was also assessed. To further probe the role of CTD-2547G23.4 in HCC cell cycle, lentivirus-mediated small interfering RNA was applied to silence CTD-2547G23.4 expression in Huh-7 cell line. In addition, the related genes of CTD-2547G23.4 gathered from The Atlas of Noncoding RNAs in Cancer (TANRIC) database and Multi Experiment Matrix (MEM) were assessed with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes, Protein Analysis Through Evolutionary Relationships and protein–protein interaction (PPI) networks.ResultsCTD-2547G23.4 expression was remarkably higher in 370 HCC tissue samples than that in adjacent non-tumour liver tissues (48.762 ± 27.270 vs. 14.511 ± 8.341, P < 0.001) from TCGA dataset. The relative expression level of CTD-2547G23.4 in HCC was consistently higher than that in adjacent non-cancerous tissues (2.464 ± 0.833 vs. 1.813 ± 0.784, P = 0.001) as assessed by real time RT-qPCR. The area under the curve of the summary receiver operating characteristic curve was 0.8720 based on TCGA, qRT-PCR and GEO data. Further analysis indicated that the increased expression levels of CTD-2547G23.4 were associated with the neoplasm histologic grade and vascular tumour cell type. The expression of CTD-2547G23.4 was significantly downregulated in CTD-2547G23.4 knockdown cells. Moreover, cell cycle analysis revealed that CTD-2547G23.4 depletion in Huh-7 cell line led to S phase arrest. Furthermore, 314 related genes identified by TANRIC and MEM databases were processed with a pathway analysis. The bioinformatics analysis indicated that CTD-2547G23.4 might play a key role in the progress of HCC through four hub genes, SRC, CREBBP, ADCY8 and PPARA.ConclusionsCollectively, we put forward the hypothesis that the novel lncRNA CTD-2547G23.4 may act as an exceptional clinical index and promote the HCC tumourigenesis and progression via various related genes.
Highlights
Dysregulated expression of long non-coding RNAs has been reported in the pathogenesis and progression of multiple cancers, including hepatocellular carcinoma (HCC)
Fur‐ thermore, 314 related genes identified by The Atlas of Noncoding RNAs in Cancer (TANRIC) and Multi Experiment Matrix (MEM) databases were processed with a pathway analysis
Collectively, we put forward the hypothesis that the novel long non-coding RNA (lncRNA) CTD-2547G23.4 may act as an exceptional clinical index and promote the Hepatocellular carcinoma (HCC) tumourigenesis and progression via various related genes
Summary
Dysregulated expression of long non-coding RNAs (lncRNAs) has been reported in the pathogenesis and progression of multiple cancers, including hepatocellular carcinoma (HCC). We aimed to clarify the expression pattern and clinical value of CTD2547G23.4 and to investigate the prospective regulatory mechanism via bioinformatics analysis in HCC. The number of new cases of HCC is increasing with each passing year. Extensive research has focused on new biomarkers associated with HCC diagnosis, prognosis, and evaluation of treatment efficacy [7,8,9,10,11]. The identification of a novel reliable biomarker and further investigation of the molecular mechanisms for HCC, which could boost the diagnostic value and survival prediction, are imperative
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