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      MicroRNAs in glioblastoma multiforme pathogenesis and therapeutics

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          Abstract

          Glioblastoma multiforme (GBM) is the most common and lethal cancer of the adult brain, remaining incurable with a median survival time of only 15 months. In an effort to identify new targets for GBM diagnostics and therapeutics, recent studies have focused on molecular phenotyping of GBM subtypes. This has resulted in mounting interest in microRNAs (miRNAs) due to their regulatory capacities in both normal development and in pathological conditions such as cancer. miRNAs have a wide range of targets, allowing them to modulate many pathways critical to cancer progression, including proliferation, cell death, metastasis, angiogenesis, and drug resistance. This review explores our current understanding of miRNAs that are differentially modulated and pathologically involved in GBM as well as the current state of miRNA‐based therapeutics. As the role of miRNAs in GBM becomes more well understood and novel delivery methods are developed and optimized, miRNA‐based therapies could provide a critical step forward in cancer treatment.

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          MicroRNAs in cancer: small molecules with a huge impact.

          Marilena V. Iorio, Carlo Croce (2009)
          Every cellular process is likely to be regulated by microRNAs, and an aberrant microRNA expression signature is a hallmark of several diseases, including cancer. MicroRNA expression profiling has indeed provided evidence of the association of these tiny molecules with tumor development and progression. An increasing number of studies have then demonstrated that microRNAs can function as potential oncogenes or oncosuppressor genes, depending on the cellular context and on the target genes they regulate. Here we review our current knowledge about the involvement of microRNAs in cancer and their potential as diagnostic, prognostic, and therapeutic tools.
          Article 0 comments Cited 343 times – based on 0 reviews     Review now
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            miR-124 and miR-137 inhibit proliferation of glioblastoma multiforme cells and induce differentiation of brain tumor stem cells

            Joachim Silber, Daniel A Lim, Claudia Petritsch … (2008)
            Background Glioblastoma multiforme (GBM) is an invariably fatal central nervous system tumor despite treatment with surgery, radiation, and chemotherapy. Further insights into the molecular and cellular mechanisms that drive GBM formation are required to improve patient outcome. MicroRNAs are emerging as important regulators of cellular differentiation and proliferation, and have been implicated in the etiology of a variety of cancers, yet the role of microRNAs in GBM remains poorly understood. In this study, we investigated the role of microRNAs in regulating the differentiation and proliferation of neural stem cells and glioblastoma-multiforme tumor cells. Methods We used quantitative RT-PCR to assess microRNA expression in high-grade astrocytomas and adult mouse neural stem cells. To assess the function of candidate microRNAs in high-grade astrocytomas, we transfected miR mimics to cultured-mouse neural stem cells, -mouse oligodendroglioma-derived stem cells, -human glioblastoma multiforme-derived stem cells and -glioblastoma multiforme cell lines. Cellular differentiation was assessed by immunostaining, and cellular proliferation was determined using fluorescence-activated cell sorting. Results Our studies revealed that expression levels of microRNA-124 and microRNA-137 were significantly decreased in anaplastic astrocytomas (World Health Organization grade III) and glioblastoma multiforme (World Health Organization grade IV) relative to non-neoplastic brain tissue (P < 0.01), and were increased 8- to 20-fold during differentiation of cultured mouse neural stem cells following growth factor withdrawal. Expression of microRNA-137 was increased 3- to 12-fold in glioblastoma multiforme cell lines U87 and U251 following inhibition of DNA methylation with 5-aza-2'-deoxycytidine (5-aza-dC). Transfection of microRNA-124 or microRNA-137 induced morphological changes and marker expressions consistent with neuronal differentiation in mouse neural stem cells, mouse oligodendroglioma-derived stem cells derived from S100β-v-erbB tumors and cluster of differentiation 133+ human glioblastoma multiforme-derived stem cells (SF6969). Transfection of microRNA-124 or microRNA-137 also induced G1 cell cycle arrest in U251 and SF6969 glioblastoma multiforme cells, which was associated with decreased expression of cyclin-dependent kinase 6 and phosphorylated retinoblastoma (pSer 807/811) proteins. Conclusion microRNA-124 and microRNA-137 induce differentiation of adult mouse neural stem cells, mouse oligodendroglioma-derived stem cells and human glioblastoma multiforme-derived stem cells and induce glioblastoma multiforme cell cycle arrest. These results suggest that targeted delivery of microRNA-124 and/or microRNA-137 to glioblastoma multiforme tumor cells may be therapeutically efficacious for the treatment of this disease.
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              microRNA-7 inhibits the epidermal growth factor receptor and the Akt pathway and is down-regulated in glioblastoma.

              Benjamin Kefas, Jakub Godlewski, Laurey Comeau … (2008)
              microRNAs are noncoding RNAs inhibiting expression of numerous target genes, and a few have been shown to act as oncogenes or tumor suppressors. We show that microRNA-7 (miR-7) is a potential tumor suppressor in glioblastoma targeting critical cancer pathways. miR-7 potently suppressed epidermal growth factor receptor expression, and furthermore it independently inhibited the Akt pathway via targeting upstream regulators. miR-7 expression was down-regulated in glioblastoma versus surrounding brain, with a mechanism involving impaired processing. Importantly, transfection with miR-7 decreased viability and invasiveness of primary glioblastoma lines. This study establishes miR-7 as a regulator of major cancer pathways and suggests that it has therapeutic potential for glioblastoma.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancer Med
                Journal ID (iso-abbrev): Cancer Med
                Journal ID (doi): 10.1002/(ISSN)2045-7634
                Journal ID (publisher-id): CAM4
                Title: Cancer Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2045-7634
                Publication date (Electronic): 10 June 2016
                Publication date Collection: August 2016
                Volume: 5
                Issue: 8 ( doiID: 10.1002/cam4.2016.5.issue-8 )
                Pages: 1917-1946
                Affiliations
                [ 1 ] Division of Science and Mathematics Cancer Research LaboratoryUniversity of the District of Columbia Washington District of Columbia 20008
                [ 2 ]Groton School Groton Massachusetts 01450
                [ 3 ] Department of Neurology and PathologyGeorgetown University Washington District of Columbia 20057
                [ 4 ] Lombardi Comprehensive Cancer CenterGeorgetown University Washington District of Columbia 20057
                [ 5 ] Division of Cancer Control and Population SciencesNational Cancer Institute (NCI) National Institutes of Health (NIH) Rockville Maryland 20850
                Author notes
                [*] [* ] Correspondence

                Deepak Kumar, Cancer Research Laboratory, Division of Science and Mathematics, University of the District of Columbia, 4200 Connecticut Avenue, NW, Washington, DC 20008. Tel: 202 274 5937; Fax: 202 274 7466; E‐mail: dkumar@ 123456udc.edu

                Article
                Publisher ID: CAM4775
                DOI: 10.1002/cam4.775
                PMC ID: 4971921
                PubMed ID: 27282910
                SO-VID: 7108b74c-0d2e-4952-85b5-c914e31acecc
                Copyright © © 2016 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 29 January 2016
                Date revision received : 05 April 2016
                Date accepted : 14 April 2016
                Page count
                Pages: 30
                Funding
                Funded by: National Cancer Institute
                Award ID: CA141935
                Award ID: CA162264
                Award ID: CA194730
                Categories
                Subject: Review
                Subject: Clinical Cancer Research
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                component-id cam4775
                cover-date August 2016
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:03.08.2016

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cancer therapy,microrna,glioblastoma multiforme
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cancer therapy, microrna, glioblastoma multiforme

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