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      HDAC2‐dependent miRNA signature in acute myeloid leukemia

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          Abstract

          Acute myeloid leukemia (AML) arises from a complex sequence of biological and finely orchestrated events that are still poorly understood. Increasingly, epigenetic studies are providing exciting findings that may be exploited in promising and personalized cutting‐edge therapies. A more appropriate and broader screening of possible players in cancer could identify a master molecular mechanism in AML. Here, we build on our previously published study by evaluating a histone deacetylase ( HDAC) 2‐mediated miRNA regulatory network in U937 leukemic cells. Following a comparative miRNA profiling analysis in genetically and enzymatically HDAC2‐downregulated AML cells, we identified miR‐96‐5p and miR‐92a‐3p as potential regulators in AML etiopathology by targeting defined genes. Our findings support the potentially beneficial role of alternative physiopathological interventions.

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          Induction of HDAC2 expression upon loss of APC in colorectal tumorigenesis.

          Ping Zhu, Elke Martin, Jörg Mengwasser … (2004)
          Inappropriate transcriptional repression involving histone deacetylases (HDACs) is a prominent cause for the development of leukemia. We now identify faulty expression of a specific mediator of transcriptional repression in a solid tumor. Loss of the adenomatosis polyposis coli (APC) tumor suppressor induces HDAC2 expression depending on the Wnt pathway and c-Myc. Increased HDAC2 expression is found in the majority of human colon cancer explants, as well as in intestinal mucosa and polyps of APC-deficient mice. HDAC2 is required for, and sufficient on its own to prevent, apoptosis of colonic cancer cells. Interference with HDAC2 by valproic acid largely diminishes adenoma formation in APC(min) mice. These findings point toward HDAC2 as a particularly relevant potential target in cancer therapy.
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            Acute Myeloid Leukemia: A Concise Review

            Jennifer N. Saultz, Ramiro Garzon (2016)
            Acute myeloid leukemia (AML) is a heterogeneous clonal disorder characterized by immature myeloid cell proliferation and bone marrow failure. Cytogenetics and mutation testing remain a critical prognostic tool for post induction treatment. Despite rapid advances in the field including new drug targets and increased understanding of the biology, AML treatment remains unchanged for the past three decades with the majority of patients eventually relapsing and dying of the disease. Allogenic transplant remains the best chance for cure for patients with intermediate or high risk disease. In this review, we discuss the landmark genetic studies that have improved outcome prediction and novel therapies.
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              The prognostic and functional role of microRNAs in acute myeloid leukemia.

              Krzysztof Mrózek, Guido Marcucci, D Bloomfield … (2011)
              Expression of microRNAs, a new class of noncoding RNAs that hybridize to target messenger RNA and regulate their translation into proteins, has been recently demonstrated to be altered in acute myeloid leukemia (AML). Distinctive patterns of increased expression and/or silencing of multiple microRNAs (microRNA signatures) have been associated with specific cytogenetic and molecular subsets of AML. Changes in the expression of several microRNAs altered in AML have been shown to have functional relevance in leukemogenesis, with some microRNAs acting as oncogenes and others as tumor suppressors. Both microRNA signatures and a single microRNA (ie, miR-181a) have been shown to supply prognostic information complementing that gained from cytogenetics, gene mutations, and altered gene expression. Moreover, it has been demonstrated experimentally that antileukemic effects can be achieved by modulating microRNA expression by pharmacologic agents and/or increasing low endogenous levels of microRNAs with tumor suppressor function by synthetic microRNA oligonucleotides, or down-regulating high endogenous levels of leukemogenic microRNAs by antisense oligonucleotides (antagomirs). Therefore, it is reasonable to predict the development of novel microRNA-based therapeutic approaches in AML. We review herein results of current studies analyzing changes of microRNA expression in AML and discuss their potential biologic, diagnostic, and prognostic relevance.
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                Author and article information

                Contributors
                Lucia Altucci: lucia.altucci@unicampania.it
                Journal
                Journal ID (nlm-ta): FEBS Lett
                Journal ID (iso-abbrev): FEBS Lett
                Journal ID (doi): 10.1002/(ISSN)1873-3468
                Journal ID (publisher-id): FEB2
                Title: Febs Letters
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0014-5793
                ISSN (Electronic): 1873-3468
                Publication date (Electronic): 19 July 2019
                Publication date (Print): September 2019
                Volume: 593
                Issue: 18 ( doiID: 10.1002/feb2.v593.18 )
                Pages: 2574-2584
                Affiliations
                [ 1 ] IRCCS, SDN Naples Italy
                [ 2 ] Department of Precision Medicine University of Campania “L. Vanvitelli” Naples Italy
                [ 3 ]Present address: Institute for Applied Mathematics “Mauro Picone” National Research Council Naples Italy
                Author notes
                [*] [* ] Correspondence

                L. Altucci, Università degli Studi della Campania “L. Vanvitelli”, Vico L. De Crecchio 7, Napoli 80138, Italy

                Tel: +39 0815667569

                E‐mail: lucia.altucci@ 123456unicampania.it

                Article
                Publisher ID: FEB213521
                DOI: 10.1002/1873-3468.13521
                PMC ID: 6790563
                PubMed ID: 31254352
                SO-VID: ade58ca9-221e-4f11-8163-d622053a98b5
                Copyright © © 2019 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 28 May 2019
                Date revision received : 11 June 2019
                Date accepted : 27 June 2019
                Page count
                Figures: 6, Tables: 5, Pages: 11, Words: 6386
                Funding
                Funded by: VALERE: Vanvitelli per la Ricerca
                Funded by: AIRC , open-funder-registry 10.13039/501100005010;
                Award ID: 17217
                Funded by: Campania Regional Government FASE2: IDEAL
                Award ID: CUP B53D18000080007
                Funded by: Campania Regional Government Lotta Alle Patologie Oncologiche, iCURE
                Award ID: CUP B21C17000030007
                Funded by: MIUR Proof of Concept EpiCURE
                Categories
                Subject: Research Article
                Subject: Research Articles
                Subject: Regulation of Gene Expression
                Custom metadata
                source-schema-version-number 2.0
                cover-date September 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.0 mode:remove_FC converted:14.10.2019

                ScienceOpen disciplines: Molecular biology
                Keywords: epigenetics,hdac2,immunoregulation,leukemia,mirna,saha
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: epigenetics, hdac2, immunoregulation, leukemia, mirna, saha

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