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Upregulation of long noncoding RNA MIAT in aggressive form of chronic lymphocytic leukemias.
Sattari, Arash; Siddiqui, Hasan; Moshiri, Farzaneh; Ngankeu, Apollinaire; Nakamura, Tatsuya; Kipps, Thomas J; Croce, Carlo M.
Afiliação
  • Sattari A; Department of Molecular Virology, Immunology, and Medical Genetics and Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
  • Siddiqui H; School of Medicine and Surgery, Department of Public Health and Community Medicine, University of Verona, Verona, Italy.
  • Moshiri F; Department of Medicine, Faculty of Medical sciences, Gorgan Branch, Islamic Azad University, Gorgan, Iran.
  • Ngankeu A; Department of Molecular Virology, Immunology, and Medical Genetics and Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
  • Nakamura T; Center for Childhood Cancer & Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
  • Kipps TJ; Department of Molecular Virology, Immunology, and Medical Genetics and Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
  • Croce CM; Department of Morphology, Experimental Medicine and Surgery, Section of Pathology, Oncology and Experimental Biology, University of Ferrara, Ferrara, Italy.
Oncotarget ; 7(34): 54174-54182, 2016 08 23.
Article em En | MEDLINE | ID: mdl-27527866
ABSTRACT
Long noncoding RNAs (lncRNAs) are non-proten-coding transcripts of more than 200 nucleotides generated by RNA polymerase II and their expressions are tightly regulated in cell type specific- and/or cellular differential stage specific- manner. MIAT, originally isolated as a candidate gene for myocardial infarction, encodes lncRNA (termed MIAT). Here, we determined the expression level of MIAT in established leukemia/lymphoma cell lines and found its upregulation in lymphoid but not in myeloid cell lineage with mature B cell phenotype. MIAT expression level was further determined in chronic lymphocytic leukemias (CLL), characterized by expansion of leukemic cells with mature B phenotype, to demonstrate relatively high occurrence of MIAT upregulation in aggressive form of CLL carrying either 17p-deletion, 11q-deletion, or Trisomy 12 over indolent form carrying 13p-deletion. Furthermore, we show that MIAT constitutes a regulatory loop with OCT4 in malignant mature B cell, as was previously reported in mouse pulripotent stem cell, and that both molecules are essential for cell survival.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Leucemia Linfocítica Crônica de Células B / RNA Longo não Codificante Limite: Humans Idioma: En Revista: Oncotarget Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Leucemia Linfocítica Crônica de Células B / RNA Longo não Codificante Limite: Humans Idioma: En Revista: Oncotarget Ano de publicação: 2016 Tipo de documento: Article