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      Targeted inhibition of mRNA translation initiation factors as a novel therapeutic strategy for mature B-cell neoplasms

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          Abstract

          Cancer development is frequently associated with dysregulation of mRNA translation to enhance both increased global protein synthesis and translation of specific mRNAs encoding oncoproteins. Thus, targeted inhibition of mRNA translation is viewed as a promising new approach for cancer therapy. In this article we review current progress in investigating dysregulation of mRNA translation initiation in mature B-cell neoplasms, focusing on chronic lymphocytic leukemia, follicular lymphoma and diffuse large B-cell lymphoma. We discuss mechanisms and regulation of mRNA translation, potential pathways by which genetic alterations and the tumor microenvironment alters mRNA translation in malignant B cells, preclinical evaluation of drugs targeted against specific eukaryotic initiation factors and current progress towards clinical development. Overall, inhibition of mRNA translation initiation factors is an exciting and promising area for development of novel targeted anti-tumor drugs.

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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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            MYC as a regulator of ribosome biogenesis and protein synthesis.

            Jan van Riggelen, Alper Yetil, Dean Felsher (2010)
            MYC regulates the transcription of thousands of genes required to coordinate a range of cellular processes, including those essential for proliferation, growth, differentiation, apoptosis and self-renewal. Recently, MYC has also been shown to serve as a direct regulator of ribosome biogenesis. MYC coordinates protein synthesis through the transcriptional control of RNA and protein components of ribosomes, and of gene products required for the processing of ribosomal RNA, the nuclear export of ribosomal subunits and the initiation of mRNA translation. We discuss how the modulation of ribosome biogenesis by MYC may be essential to its physiological functions as well as its pathological role in tumorigenesis.
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              RNA G-quadruplexes cause eIF4A-dependent oncogene translation in cancer

              Andrew L. Wolfe, Kamini Singh, Yi Zhong … (2014)
              The translational control of oncoprotein expression is implicated in many cancers. Here we report an eIF4A/DDX2 RNA helicase-dependent mechanism of translational control that contributes to oncogenesis and underlies the anticancer effects of Silvestrol and related compounds. For example, eIF4A promotes T-ALL development in vivo and is required for leukaemia maintenance. Accordingly, inhibition of eIF4A with Silvestrol has powerful therapeutic effects in vitro and in vivo. We use transcriptome-scale ribosome footprinting to identify the hallmarks of eIF4A-dependent transcripts. These include 5′UTR sequences such as the 12-mer guanine quartet (CGG)4 motif that can form RNA G-quadruplex structures. Notably, among the most eIF4A-dependent and Silvestrol-sensitive transcripts are a number of oncogenes, super-enhancer associated transcription factors, and epigenetic regulators. Hence, the 5′UTRs of selected cancer genes harbour a targetable requirement for the eIF4A RNA helicase.
              Article 0 comments Cited 285 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 101770662
                Journal ID (nlm-ta): Explor Target Antitumor Ther
                Journal ID (iso-abbrev): Explor Target Antitumor Ther
                Title: Exploration of targeted anti-tumor therapy
                ISSN (Electronic): 2692-3114
                Publication date Nihms-submitted: 03 September 2020
                Publication date (Electronic): 29 February 2020
                Publication date PMC-release: 10 September 2020
                Volume: 1
                Pages: 3-25
                Affiliations
                Cancer Research UK Centre, Cancer Sciences, Faculty of Medicine, University of Southampton, SO16 6YD Southampton, United Kingdom
                Author notes
                [* ] Correspondence: Graham Packham, Cancer Research UK Centre, Cancer Sciences, Faculty of Medicine, University of Southampton, SO16 6YD Southampton, United Kingdom. gpackham@ 123456soton.ac.uk

                Academic Editor: Nicola Normanno, Istituto Nazionale Tumori “Fondazione Pascale” Via Mariano Semmola, Italy

                Author information
                https://orcid.org/0000-0002-9232-5691
                Article
                Manuscript ID: EMS94606
                DOI: 10.37349/etat.2020.00002
                PMC ID: 7116065
                PubMed ID: 32924027
                SO-VID: 538f4294-8349-4b06-b999-bddf8d7e2b68
                License:

                This is an Open Access article licensed under a Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Categories
                Subject: Article

                Keywords: mrna translation,initiation,lymphoma,leukemia,inhibitor,drug
                Data availability:
                Keywords: mrna translation, initiation, lymphoma, leukemia, inhibitor, drug

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