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      miR-19b regulates hTERT mRNA expression through targeting PITX1 mRNA in melanoma cells

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          Abstract

          Human telomerase reverse transcriptase ( hTERT) plays a crucial role in cancer development. We previously identified paired-like homeodomain1 ( PITX1) as an hTERT suppressor gene. However, the underlying mechanisms that are involved in the regulation of PITX1 remain unknown. Here, we report that the microRNA-19b (miR-19b) regulates hTERT expression and cell proliferation through inhibition of PITX1. Compared with normal melanocyte cells, miR-19b expression was higher in most melanoma cells and was accompanied by downregulation of PITX1. Moreover, overexpression of miR-19b inhibited PITX1 mRNA translation through a miR-19b binding site within the 3′UTR of the PITX1 mRNA. Our combined findings indicate the participation of miR-19b as a novel upstream effector of hTERT transcription via direct targeting of PITX1.

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          PI3K signalling: the path to discovery and understanding.

          Bart Vanhaesebroeck, Len Stephens, Phillip N Hawkins (2012)
          Over the past two decades, our understanding of phospoinositide 3-kinases (PI3Ks) has progressed from the identification of an enzymatic activity associated with growth factors, GPCRs and certain oncogene products to a disease target in cancer and inflammation, with PI3K inhibitors currently in clinical trials. Elucidation of PI3K-dependent networks led to the discovery of the phosphoinositide-binding PH, PX and FYVE domains as conduits of intracellular lipid signalling, the determination of the molecular function of the tumour suppressor PTEN and the identification of AKT and mTOR protein kinases as key regulators of cell growth. Here we look back at the main discoveries that shaped the PI3K field.
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            miR-19 is a key oncogenic component of mir-17-92.

            Virginie Olive, Margaux J Bennett, James C. Walker … (2009)
            Recent studies have revealed the importance of multiple microRNAs (miRNAs) in promoting tumorigenesis, among which mir-17-92/Oncomir-1 exhibits potent oncogenic activity. Genomic amplification and elevated expression of mir-17-92 occur in several human B-cell lymphomas, and enforced mir-17-92 expression in mice cooperates with c-myc to promote the formation of B-cell lymphomas. Unlike classic protein-coding oncogenes, mir-17-92 has an unconventional gene structure, where one primary transcript yields six individual miRNAs. Here, we functionally dissected the individual components of mir-17-92 by assaying their tumorigenic potential in vivo. Using the Emu-myc model of mouse B-cell lymphoma, we identified miR-19 as the key oncogenic component of mir-17-92, both necessary and sufficient for promoting c-myc-induced lymphomagenesis by repressing apoptosis. The oncogenic activity of miR-19 is at least in part due to its repression of the tumor suppressor Pten. Consistently, miR-19 activates the Akt-mTOR (mammalian target of rapamycin) pathway, thereby functionally antagonizing Pten to promote cell survival. Our findings reveal the essential role of miR-19 in mediating the oncogenic activity of mir-17-92, and implicate the functional diversity of mir-17-92 components as the molecular basis for its pleiotropic effects during tumorigenesis.
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              Wnt/β-catenin signaling regulates telomerase in stem cells and cancer cells.

              Katrin Hoffmeyer, Angelo Raggioli, Stefan Rudloff … (2012)
              Telomerase activity controls telomere length and plays a pivotal role in stem cells, aging, and cancer. Here, we report a molecular link between Wnt/β-catenin signaling and the expression of the telomerase subunit Tert. β-Catenin-deficient mouse embryonic stem (ES) cells have short telomeres; conversely, ES cell expressing an activated form of β-catenin (β-cat(ΔEx3/+)) have long telomeres. We show that β-catenin regulates Tert expression through the interaction with Klf4, a core component of the pluripotency transcriptional network. β-Catenin binds to the Tert promoter in a mouse intestinal tumor model and in human carcinoma cells. We uncover a previously unknown link between the stem cell and oncogenic potential whereby β-catenin regulates Tert expression, and thereby telomere length, which could be critical in human regenerative therapy and cancer.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 03 February 2015
                Publication date Collection: 2015
                Volume: 5
                Electronic Location Identifier: 8201
                Affiliations
                [1 ]Department of Biomedical Science, Institute of Regenerative Medicine and Biofunction, Graduate School of Medical Science, Tottori University , Yonago, Tottori 683-8503, Japan
                [2 ]Division of Functional Genomics, Research Center for Bioscience and Technology, Tottori University , Yonago, Tottori 683-8503, Japan
                [3 ]Division of Pathological Biochemistry, School of Life Science, Faculty of Medicine, Tottori University , Yonago, Tottori 683-8503, Japan
                [4 ]Chromosome Engineering Research Center, Tottori University , Yonago, Tottori 683-8503, Japan
                Author notes
                Article
                Publisher Item ID: srep08201
                DOI: 10.1038/srep08201
                PMC ID: 4314654
                PubMed ID: 25643913
                SO-VID: 5e5bed70-cc73-44c1-9615-f70ee35e5635
                Copyright © Copyright © 2015, Macmillan Publishers Limited. All rights reserved
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 13 October 2014
                Date accepted : 12 January 2015
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                Subject: Article

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