Clinicopathological role of miR-30a-5p in hepatocellular carcinoma tissues and prediction of its function with bioinformatics analysis
Authors Huang W, Chen Z, He R, Wu Y, Yin S, Liang X, Chen G, Yang H, Peng Z, Yang L
Received 26 April 2016
Accepted for publication 19 May 2016
Published 12 August 2016 Volume 2016:9 Pages 5061—5071
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Narasimha Reddy Parine
Peer reviewer comments 2
Editor who approved publication: Professor Min Li
Wen-Ting Huang,1,* Zu-xuan Chen,2,* Rong-quan He,2 Yu-zhuang Wu,1 Shu-ya Yin,1 Xiao-na Liang,1 Gang Chen,1 Hong Yang,3 Zhi-gang Peng,2,* Li-hua Yang2,*
1Department of Pathology, 2Department of Medical Oncology, 3Department of Ultrasonography, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, People’s Republic of China
*These authors contributed equally to this work
Background: It has been reported that deregulation or dysfunction of microRNAs (miRNAs) plays an essential part in the hepatocarcinogenesis. However, the contribution and mechanism of microRNA-30a-5p (miR-30a-5p) in hepatocellular carcinoma (HCC) remains largely unknown. Therefore, our aim was to investigate the clinicopathological role of miR-30a-5p in HCC tissues and explore its potential pathways in this study.
Methods: The expression of miR-30a-5p was measured in 95 HCC and adjacent noncancer tissues by real-time reverse transcription quantitative polymerase chain reaction. The relationship between miR-30a-5p expression levels and clinicopathological parameters was also analyzed. Furthermore, the potential target genes of miR-30a-5p were collected via online prediction and literature searching. Gene ontology and pathway enrichment analyses were used to identify the possible function of miR-30a-5p in HCC.
Results: Compared with adjacent noncancer tissues (2.23±0.77), expression level of miR-30a-5p was significantly lower in HCC tissues (1.26±0.66, P<0.001). MiR-30a-5p expression was evidently correlated with tumor nodes, metastasis, tumor–node–metastasis stage, portal vein tumor embolus, vascular invasion, and status of tumor capsule (all P<0.05). A total of 878 genes were finally used for the biological informatics analyses. These prospective target genes were highly enriched in various key pathways, for instance, Ubiquitin-mediated proteolysis, Axon guidance, Neurotrophin signaling pathway, Amyotrophic lateral sclerosis, and ErbB signaling pathway.
Conclusion: In conclusion, this study clarifies that the downregulation of miRNA-30a-5p might play a vital part in the incidence and progression of HCC via targeting various prospective genes and pathways. Future validation is required to further explore the prospective molecular mechanism of miR-30a-5p in HCC.
Keywords: miR-30a-5p, hepatocellular carcinoma, progression, target genes, gene ontology analysis, pathway analysis
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