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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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      The role of miR-29b in cancer: regulation, function, and signaling

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          Abstract

          MicroRNAs (miRNAs) are endogenous small non-coding RNAs with the capacity to regulate gene expression post-transcriptionally. The miRNA-29 family consists of miR-29a, miR-29b, and miR-29c, among which miR-29b is the most highly expressed and is found at two genomic loci. Recently, numerous studies have demonstrated that aberrant expression of miR-29b is common in the majority of human cancers. miR-29b is known to critically affect cancer progression by functioning as a tumor suppressor. However, it may also act as an oncogene under certain conditions. In this review, we illustrate the role of miR-29b in cancer regulation, function, and signaling. This is the first review highlighting the role of miR-29b in cancer. Our review aims to summarize the effects of miR-29b on cancer activity and its interactions with target genes and signaling pathways, as well as to provide therapeutic implications for overcoming cancer chemoresistance.

          Most cited references54

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          Widespread microRNA repression by Myc contributes to tumorigenesis.

          Tsung-Cheng Chang, Duonan Yu, Yun-Sil Lee … (2008)
          The c-Myc oncogenic transcription factor (Myc) is pathologically activated in many human malignancies. Myc is known to directly upregulate a pro-tumorigenic group of microRNAs (miRNAs) known as the miR-17-92 cluster. Through the analysis of human and mouse models of B cell lymphoma, we show here that Myc regulates a much broader set of miRNAs than previously anticipated. Unexpectedly, the predominant consequence of activation of Myc is widespread repression of miRNA expression. Chromatin immunoprecipitation reveals that much of this repression is likely to be a direct result of Myc binding to miRNA promoters. We further show that enforced expression of repressed miRNAs diminishes the tumorigenic potential of lymphoma cells. These results demonstrate that extensive reprogramming of the miRNA transcriptome by Myc contributes to tumorigenesis.
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            MicroRNAs as oncogenes and tumor suppressors.

            Chang-Zheng Chen (2005)
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              mir-29 regulates Mcl-1 protein expression and apoptosis.

              J L Mott, S. Kobayashi, S Bronk … (2007)
              Cellular expression of Mcl-1, an anti-apoptotic Bcl-2 family member, is tightly regulated. Recently, Bcl-2 expression was shown to be regulated by microRNAs, small endogenous RNA molecules that regulate protein expression through sequence-specific interaction with messenger RNA. By analogy, we reasoned that Mcl-1 expression may also be regulated by microRNAs. We chose human immortalized, but non-malignant, H69 cholangiocyte and malignant KMCH cholangiocarcinoma cell lines for these studies, because Mcl-1 is dysregulated in cells with the malignant phenotype. By in silico analysis, we identified a putative target site in the Mcl-1 mRNA for the mir-29 family, and found that mir-29b was highly expressed in cholangiocytes. Interestingly, mir-29b was downregulated in malignant cells, consistent with Mcl-1 protein upregulation. Enforced mir-29b expression reduced Mcl-1 protein expression in KMCH cells. This effect was direct, as mir-29b negatively regulated the expression of an Mcl-1 3' untranslated region (UTR)-based reporter construct. Enforced mir-29b expression reduced Mcl-1 cellular protein levels and sensitized the cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) cytotoxicity. Transfection of non-malignant cells (that express high levels of mir-29) with a locked-nucleic acid antagonist of mir-29b increased Mcl-1 levels and reduced TRAIL-mediated apoptosis. Thus mir-29 is an endogenous regulator of Mcl-1 protein expression, and thereby, apoptosis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Onco Targets Ther
                Journal ID (iso-abbrev): Onco Targets Ther
                Journal ID (publisher-id): OncoTargets and Therapy
                Title: OncoTargets and therapy
                Publisher: Dove Medical Press
                ISSN (Electronic): 1178-6930
                Publication date Collection: 2015
                Publication date (Electronic): 03 March 2015
                Volume: 8
                Pages: 539-548
                Affiliations
                [1 ]Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, People’s Republic of China
                [2 ]Department of Urology, The Central Hospital of Changsha, Changsha, People’s Republic of China
                [3 ]Department of Urology, The Central Hospital of Changsha, Changsha, People’s Republic of China
                Author notes
                Correspondence: Jin-rui Yang, Department of Urology, The Second Xiangya Hospital, Central South University, Changsha 410011, People’s Republic of China, Email yangjr06@ 123456163.com
                Fa-jun Fu, Department of Urology, The Central Hospital of Changsha, Changsha, 410004, People’s Republic of China, Email 675390797@ 123456qq.com

                *These authors contributed equally to this work

                Article
                Publisher ID: ott-8-539
                DOI: 10.2147/OTT.S75899
                PMC ID: 4354468
                PubMed ID: 25767398
                SO-VID: d52229d5-52a2-4ff1-aed1-8732cd2055aa
                Copyright © © 2015 Yan et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License
                License:

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: mir-29b,cancer,biological function,oncogene,tumor promoter,chemoresistance
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: mir-29b, cancer, biological function, oncogene, tumor promoter, chemoresistance

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