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.

Asian Pac J Cancer Prev, 15 (21), 9137-9142 IntroductionBladder urothelial carcinoma (BUC) is the fifth most common cancer worldwide, with an estimated incidence of 73, 510 cases and 14, 880 deaths in the United States in 2012. In China, the morbidity of urothelial carcinoma is 6.61/100,000, ranked the ninth in all malignant tumors (O'Keeffe et al., 2008;Yang et al., 2011;Siegel et al., 2012;Bracha et al., 2014). The decoy receptor 3 (DcR3), locating on chromosome 20q13, is a member of the tumor necrosis factor receptor (TNFR) superfamily. Previously, we have reported the overexpression of DcR3 mRNA and protein in sera or tissues of several human malignancies, including hepatocellular carcinoma, gastric carcinoma and glioma (Chen and Luo, 2008a;2008b;Chen et al., 2010;Huang et al., 2014). DcR3 has been considered as an oncogene for the aforementioned malignancies. So far, there has been only one report studying the relationship between DcR3 and urothelial carcinoma (UC). Yamana et al. (2005) investigated the amplification and protein expression of DcR3 in the tissues and cell lines of UC by using real-time quantitative PCR and immunohistochemistry in a small number of patients.However, no study has been performed to explore the relationship between DcR3 and progression of UC patients. Furthermore, the role of DcR3 on BUC has not been fully clarified. Thus, the aim of the current study was to explore