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      MicroRNA-552 promotes hepatocellular carcinoma progression by downregulating WIF1

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          Abstract

          MicroRNAs (miRNAs/miRs) are involved in the metastasis of hepatocellular carcinoma (HCC). In the present study, it was demonstrated that miR-552 was upregulated in HCC tissues. High miR-552 expression was associated with malignant clinicopathological features and decreased survival rates. The in vitro results indicated that miR-552 overexpression promoted migration, invasion and epithelial-mesenchymal transition in Hep3B cells. However, the knockdown of miR-552 inhibited its oncogenic roles in Huh-7 cells. Additionally, Wnt inhibitory factor 1 (WIF1) was demonstrated to be a direct target of miR-552 in Hep3B and Huh-7 cells. Additional experiments identified that miR-552 promotes β-catenin expression by increasing the phosphorylation of GSK3β at Ser9. In conclusion, the results suggested that miR-552 may promote HCC progression by blocking WIF1-mediated GSK3β dephosphorylation. miR-552 may be a biomarker for predicting the outcomes of patients with HCC.

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          Nuclear functions of mammalian MicroRNAs in gene regulation, immunity and cancer

          Hongyu Liu, Cheng Lei, Qin He … (2018)
          MicroRNAs (miRNAs) are endogenous non-coding RNAs that contain approximately 22 nucleotides. They serve as key regulators in various biological processes and their dysregulation is implicated in many diseases including cancer and autoimmune disorders. It has been well established that the maturation of miRNAs occurs in the cytoplasm and miRNAs exert post-transcriptional gene silencing (PTGS) via RNA-induced silencing complex (RISC) pathway in the cytoplasm. However, numerous studies reaffirm the existence of mature miRNA in the nucleus, and nucleus-cytoplasm transport mechanism has also been illustrated. Moreover, active regulatory functions of nuclear miRNAs were found including PTGS, transcriptional gene silencing (TGS), and transcriptional gene activation (TGA), in which miRNAs bind nascent RNA transcripts, gene promoter regions or enhancer regions and exert further effects via epigenetic pathways. Based on existing interaction rules, some miRNA binding sites prediction software tools are developed, which are evaluated in this article. In addition, we attempt to explore and review the nuclear functions of miRNA in immunity, tumorigenesis and invasiveness of tumor. As a non-canonical aspect of miRNA action, nuclear miRNAs supplement miRNA regulatory networks and could be applied in miRNA based therapies.
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            miRNA Expression in Colon Polyps Provides Evidence for a Multihit Model of Colon Cancer

            Ann Oberg, Amy J French, Aaron Sarver … (2011)
            Changes in miRNA expression are a common feature in colon cancer. Those changes occurring in the transition from normal to adenoma and from adenoma to carcinoma, however, have not been well defined. Additionally, miRNA changes among tumor subgroups of colon cancer have also not been adequately evaluated. In this study, we examined the global miRNA expression in 315 samples that included 52 normal colonic mucosa, 41 tubulovillous adenomas, 158 adenocarcinomas with proficient DNA mismatch repair (pMMR) selected for stage and age of onset, and 64 adenocarcinomas with defective DNA mismatch repair (dMMR) selected for sporadic (n = 53) and inherited colon cancer (n = 11). Sporadic dMMR tumors all had MLH1 inactivation due to promoter hypermethylation. Unsupervised PCA and cluster analysis demonstrated that normal colon tissue, adenomas, pMMR carcinomas and dMMR carcinomas were all clearly discernable. The majority of miRNAs that were differentially expressed between normal and polyp were also differentially expressed with a similar magnitude in the comparison of normal to both the pMMR and dMMR tumor groups, suggesting a stepwise progression for transformation from normal colon to carcinoma. Among the miRNAs demonstrating the largest fold up- or down-regulated changes (≥4), four novel (miR-31, miR-1, miR-9 and miR-99a) and two previously reported (miR-137 and miR-135b) miRNAs were identified in the normal/adenoma comparison. All but one of these (miR-99a) demonstrated similar expression differences in the two normal/carcinoma comparisons, suggesting that these early tumor changes are important in both the pMMR- and dMMR-derived cancers. The comparison between pMMR and dMMR tumors identified four miRNAs (miR-31, miR-552, miR-592 and miR-224) with statistically significant expression differences (≥2-fold change).
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              Expression, regulation and mechanism of action of the miR-17-92 cluster in tumor cells (Review)

              Li-Li Fang, Xing-Hui Wang, Bao-Fei Sun … (2017)
              MicroRNAs (miRNAs), a class of short, single-stranded non-coding RNAs, regulate and control gene expression in eukaryotes by degrading mRNA at the post-transcriptional level. Regulation by miRNAs involves a plethora of biological processes, such as cell differentiation, proliferation, metastasis, metabolism, apoptosis, tumorigenesis and others. miRNAs also represent a powerful tool in disease diagnosis and prognosis. The miR-17-92 cluster, one of the most extensively investigated microRNA clusters, comprises six mature miRNA members, including miR-17, miR-18a, miR-19a, miR-19b, miR-20a and miR-92a. Originally identified as being involved in tumorigenesis, it is currently evident that the expression of the miR-17-92 cluster is upregulated in a wide range of tumor cells and cancer types; thus, this cluster has been identified as a potential oncogene. Considering the growing interest in the field of miR-17-92 research, we herein review recent advances in the expression and regulation of this cluster in various cancer cells, discuss the proposed mechanism of action for tumorigenesis and tumor development, and propose clinical and therapeutic applications for miR-17-92 cluster members, such as potential cancer biomarkers.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Med
                Journal ID (iso-abbrev): Int. J. Mol. Med
                Journal ID (publisher-id): IJMM
                Title: International Journal of Molecular Medicine
                Publisher: D.A. Spandidos
                ISSN (Print): 1107-3756
                ISSN (Electronic): 1791-244X
                Publication date (Print): December 2018
                Publication date (Electronic): 17 September 2018
                Publication date PMC-release: 17 September 2018
                Volume: 42
                Issue: 6
                Pages: 3309-3317
                Affiliations
                [1 ]Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi 710061
                [2 ]Department of General Surgery, Ankang People’s Hospital, Ankang, Shaanxi 725000, P.R. China
                Author notes
                Correspondence to: Professor Chang Liu, Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, 277 Yanta West Road, Xi’an, Shaanxi 710061, P.R. China, E-mail: liuchangdoctor@ 123456163.com
                Article
                Publisher ID: ijmm-42-06-3309
                DOI: 10.3892/ijmm.2018.3882
                PMC ID: 6202085
                PubMed ID: 30221686
                SO-VID: 49032f50-9766-43c0-bffa-e10c883d8cf9
                Copyright © Copyright: © Li et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 22 March 2018
                Date accepted : 04 September 2018
                Categories
                Subject: Articles

                Keywords: microrna-552,hepatocellular carcinoma,invasion,epithelial-mesenchymal transition,wnt inhibitory factor 1
                Data availability:
                Keywords: microrna-552, hepatocellular carcinoma, invasion, epithelial-mesenchymal transition, wnt inhibitory factor 1

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