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      A Systematic Review of miR-29 in Cancer

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          Abstract

          MicroRNAs (miRNA) are small non-coding RNAs (∼22 nt in length) that are known as potent master regulators of eukaryotic gene expression. miRNAs have been shown to play a critical role in cancer pathogenesis, and the misregulation of miRNAs is a well-known feature of cancer. In recent years, miR-29 has emerged as a critical miRNA in various cancers, and it has been shown to regulate multiple oncogenic processes, including epigenetics, proteostasis, metabolism, proliferation, apoptosis, metastasis, fibrosis, angiogenesis, and immunomodulation. Although miR-29 has been thoroughly documented as a tumor suppressor in the majority of studies, some controversy remains with conflicting reports of miR-29 as an oncogene. In this review, we provide a systematic overview of miR-29’s functional role in various mechanisms of cancer and introspection on the contradictory roles of miR-29.

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          Nuclear export of microRNA precursors.

          Elsebet Lund, Stephan Güttinger, Angelo Calado … (2004)
          MicroRNAs (miRNAs), which function as regulators of gene expression in eukaryotes, are processed from larger transcripts by sequential action of nuclear and cytoplasmic ribonuclease III-like endonucleases. We show that Exportin-5 (Exp5) mediates efficient nuclear export of short miRNA precursors (pre-miRNAs) and that its depletion by RNA interference results in reduced miRNA levels. Exp5 binds correctly processed pre-miRNAs directly and specifically, in a Ran guanosine triphosphate-dependent manner, but interacts only weakly with extended pre-miRNAs that yield incorrect miRNAs when processed by Dicer in vitro. Thus, Exp5 is key to miRNA biogenesis and may help coordinate nuclear and cytoplasmic processing steps.
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            Pancreatic cancers require autophagy for tumor growth.

            Shenghong Yang, Xiaoxu Wang, Gianmarco Contino … (2011)
            Macroautophagy (autophagy) is a regulated catabolic pathway to degrade cellular organelles and macromolecules. The role of autophagy in cancer is complex and may differ depending on tumor type or context. Here we show that pancreatic cancers have a distinct dependence on autophagy. Pancreatic cancer primary tumors and cell lines show elevated autophagy under basal conditions. Genetic or pharmacologic inhibition of autophagy leads to increased reactive oxygen species, elevated DNA damage, and a metabolic defect leading to decreased mitochondrial oxidative phosphorylation. Together, these ultimately result in significant growth suppression of pancreatic cancer cells in vitro. Most importantly, inhibition of autophagy by genetic means or chloroquine treatment leads to robust tumor regression and prolonged survival in pancreatic cancer xenografts and genetic mouse models. These results suggest that, unlike in other cancers where autophagy inhibition may synergize with chemotherapy or targeted agents by preventing the up-regulation of autophagy as a reactive survival mechanism, autophagy is actually required for tumorigenic growth of pancreatic cancers de novo, and drugs that inactivate this process may have a unique clinical utility in treating pancreatic cancers and other malignancies with a similar dependence on autophagy. As chloroquine and its derivatives are potent inhibitors of autophagy and have been used safely in human patients for decades for a variety of purposes, these results are immediately translatable to the treatment of pancreatic cancer patients, and provide a much needed, novel vantage point of attack.
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              Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis.

              Eva van Rooij, Lillian Sutherland, Jeffrey Thatcher … (2008)
              Acute myocardial infarction (MI) due to coronary artery occlusion is accompanied by a pathological remodeling response that includes hypertrophic cardiac growth and fibrosis, which impair cardiac contractility. Previously, we showed that cardiac hypertrophy and heart failure are accompanied by characteristic changes in the expression of a collection of specific microRNAs (miRNAs), which act as negative regulators of gene expression. Here, we show that MI in mice and humans also results in the dysregulation of specific miRNAs, which are similar to but distinct from those involved in hypertrophy and heart failure. Among the MI-regulated miRNAs are members of the miR-29 family, which are down-regulated in the region of the heart adjacent to the infarct. The miR-29 family targets a cadre of mRNAs that encode proteins involved in fibrosis, including multiple collagens, fibrillins, and elastin. Thus, down-regulation of miR-29 would be predicted to derepress the expression of these mRNAs and enhance the fibrotic response. Indeed, down-regulation of miR-29 with anti-miRs in vitro and in vivo induces the expression of collagens, whereas over-expression of miR-29 in fibroblasts reduces collagen expression. We conclude that miR-29 acts as a regulator of cardiac fibrosis and represents a potential therapeutic target for tissue fibrosis in general.
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                Author and article information

                Contributors
                Janaiah Kota
                Journal
                Journal ID (nlm-ta): Mol Ther Oncolytics
                Journal ID (iso-abbrev): Mol Ther Oncolytics
                Title: Molecular Therapy Oncolytics
                Publisher: American Society of Gene & Cell Therapy
                ISSN (Electronic): 2372-7705
                Publication date PMC-release: 31 December 2018
                Publication date Collection: 29 March 2019
                Publication date (Electronic): 31 December 2018
                Volume: 12
                Pages: 173-194
                Affiliations
                [1 ]Department of Medical and Molecular Genetics, Indiana University School of Medicine (IUSM), Indianapolis, IN, USA
                [2 ]The Melvin and Bren Simon Cancer Center, IUSM, Indianapolis, IN, USA
                Author notes
                [∗ ]Corresponding author: Janaiah Kota, Department of Medical and Molecular Genetics, Indiana University School of Medicine, 975 West Walnut Street, IB 244C, Indianapolis, IN 46202, USA. jkota@ 123456iu.edu
                [3]

                These authors contributed equally to this work.

                Article
                Publisher ID: S2372-7705(18)30048-2
                DOI: 10.1016/j.omto.2018.12.011
                PMC ID: 6369137
                PubMed ID: 30788428
                SO-VID: d9427a56-1906-4749-8c9c-63a25d35e54d
                Copyright © © 2018.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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