Abstract:
:The clinical significance of microRNA (miR)‑136‑5p in hepatocellular carcinoma (HCC) has not been verified. Therefore, in the current study, the authors aimed to explore miR‑136‑5p expression and its clinical significance in HCC, as well as to investigate its potential target genes function. The authors detected the levels of miR‑136‑5p in 101 pairs of HCC and para‑cancer tissues via reverse transcription‑quantitative polymerase chain reaction. Gene Expression Omnibus database and the Cancer Genome Atlas (TCGA) database were used to further verify the clinical significance of miR‑136‑5p expression in HCC. The target genes prediction analysis of miR‑136‑5p, natural language processing (NLP) analysis of HCC in PubMed and gene functional enrichment analysis were conducted. The miR‑136‑5p level was markedly downregulated in HCC tissue, compared to para‑non‑tumor tissue. MiR‑136‑5p expression decreased in HCC patients with metastasis (P=0.004), advance TNM stage (P<0.001), portal vein tumor embolus (P=0.007) and vaso‑invasion (P=0.003), compared with those HCC patients with non‑metastasis, early TNM stage, non‑portal vein tumor embolus and non‑vaso‑invasion, respectively. In the TCGA database, downregulated miR‑136‑5p was also observed in HCC tissue compared to normal liver tissue (P<0.001). There were 178 genes obtained from the overlap between predicted targets and NLP analysis. GO and KEGG pathway analyses revealed some significant pathways related to cancers. Downregulation of miR‑136‑5p may be responsible for the carcinogenesis and aggressiveness of HCC. miR‑136‑5p may act as an anti‑carcinoma miRNA, which is essential for HCC progression through the regulation of various signaling pathways. Thus, miR‑136‑5p interaction may provide a novel strategy for HCC treatment.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Ding H,Ye ZH,Wen DY,Huang XL,Zeng CM,Mo J,Jiang YQ,Li JJ,Cai XY,Yang H,Chen Gdoi
10.3892/mmr.2017.7275subject
Has Abstractpub_date
2017-10-01 00:00:00pages
5393-5405issue
4eissn
1791-2997issn
1791-3004journal_volume
16pub_type
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