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      CD90+ liver cancer cells modulate endothelial cell phenotype through the release of exosomes containing H19 lncRNA.

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          Abstract

          CD90+ liver cancer cells have been described as cancer stem-cell-like (CSC), displaying aggressive and metastatic phenotype. Using two different in vitro models, already described as CD90+ liver cancer stem cells, our aim was to study their interaction with endothelial cells mediated by the release of exosomes.

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          Most cited references34

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          Emerging functional and mechanistic paradigms of mammalian long non-coding RNAs

          The recent discovery that the human and other mammalian genomes produce thousands of long non-coding RNAs (lncRNAs) raises many fascinating questions. These mRNA-like molecules, which lack significant protein-coding capacity, have been implicated in a wide range of biological functions through diverse and as yet poorly understood molecular mechanisms. Despite some recent insights into how lncRNAs function in such diverse cellular processes as regulation of gene expression and assembly of cellular structures, by and large, the key questions regarding lncRNA mechanisms remain to be answered. In this review, we discuss recent advances in understanding the biology of lncRNAs and propose avenues of investigation that may lead to fundamental new insights into their functions and mechanisms of action. Finally, as numerous lncRNAs are dysregulated in human diseases and disorders, we also discuss potential roles for these molecules in human health.
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            Long non-coding RNA H19 increases bladder cancer metastasis by associating with EZH2 and inhibiting E-cadherin expression.

            lncRNA H19 is essential for human tumor growth. However, little is known about whether H19 regulates bladder cancer metastasis. Here we found that H19 levels are remarkably increased in bladder cancer tissues, and upregulated H19 promotes bladder cancer cell migration in vitro and in vivo. H19 is associated with enhancer of zeste homolog 2 (EZH2), and that this association results in Wnt/β-catenin activation and subsequent downregulation of E-cadherin. A significant negative correlation is also observed between H19 levels and E-cad levels in vivo. These data suggest that upregulated H19 enhances bladder cancer metastasis by associating with EZH2 and inhibiting E-cad expression. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
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              • Abstract: found
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              Up-regulated long non-coding RNA H19 contributes to proliferation of gastric cancer cells.

              Long non-coding RNAs (lncRNAs) have been shown to have important regulatory roles in cancer biology, and the lncRNA H19 is up-regulated in hypoxic stress and in some tumors. However, the contributions of H19 to gastric cancer remain largely unknown. In this study, we assayed the H19 expression level in gastric cancer tissues by real-time PCR, and defined the biological functions by flow cytometry and RNA immunoprecipitation. We demonstrated that H19 levels were markedly increased in gastric cancer cells and gastric cancer tissues compared with normal controls. Moreover, ectopic expression of H19 increased cell proliferation, whereas H19 siRNA treatment contributed to cell apoptosis in AGS cell line. We further verified that H19 was associated with p53, and that this association resulted in partial p53 inactivation. These data suggest an important role for H19 in the molecular etiology of gastric cancer and potential application of H19 in gastric cancer therapy. © 2012 The Authors Journal compilation © 2012 FEBS.
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                Author and article information

                Journal
                Mol. Cancer
                Molecular cancer
                Springer Science and Business Media LLC
                1476-4598
                1476-4598
                Aug 14 2015
                : 14
                Affiliations
                [1 ] Dipartimento di Biotecnologie Cellulari ed Ematologia, Sapienza University of Rome, c/o Policlinico Umberto I, V Clinica Medica Viale Regina Elena, Rome, 324-00161, Italy. alice.conigliaro@uniroma1.it.
                [2 ] Laboratory of Tissue Engineering - Innovative Technology Platforms for Tissue Engineering (PON01-00829), Rizzoli Orthopedic Institute, Palermo, Italy.
                [3 ] Dipartimento di Biopatologia e Biotecnologie Mediche, University of Palermo, Via Divisi 83-90133, Palermo, Italy.
                [4 ] Servizio di Diabetologia, Dipartimento per la cura e lo studio della patologie addominali e dei trapianti addominali, ISMETT IRCCS, Palermo, Italy.
                [5 ] Institute of Biophysics, National Research Council of Italy, Palermo, Italy.
                [6 ] Dipartimento di Biotecnologie Cellulari ed Ematologia, Sapienza University of Rome, c/o Policlinico Umberto I, V Clinica Medica Viale Regina Elena, Rome, 324-00161, Italy.
                [7 ] National Institute for Infectious Diseases L. Spallanzani, IRCCS, Rome, Italy.
                [8 ] Istituto Pasteur-Fondazione Cenci Bolognetti, Dipartimento di Biotecnologie Cellulari ed Ematologia, Sapienza University of Rome, Rome, Italy.
                [9 ] Dipartimento di Biopatologia e Biotecnologie Mediche, University of Palermo, Via Divisi 83-90133, Palermo, Italy. riccardo.alessandro@unipa.it.
                [10 ] Institute of Biomedicine and Molecular Immunology (IBIM), National Research Council of Italy, Palermo, Italy. riccardo.alessandro@unipa.it.
                Article
                10.1186/s12943-015-0426-x
                10.1186/s12943-015-0426-x
                4536801
                26272696
                8bcde8b3-7a6a-4ef0-a2d7-379faf7a47aa
                History

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