Priority Research Papers:
Upregulation of long noncoding RNA MIAT in aggressive form of chronic lymphocytic leukemias
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Abstract
Arash Sattari1,2,3, Hasan Siddiqui1,7, Farzaneh Moshiri1,4, Apollinaire Ngankeu1, Tatsuya Nakamura1, Thomas J Kipps5,6 and Carlo M. Croce1
1 Department of Molecular Virology, Immunology, and Medical Genetics and Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA
2 School of Medicine and Surgery, Department of Public Health and Community Medicine, University of Verona, Verona, Italy
3 Department of Medicine, Faculty of Medical sciences, Gorgan Branch, Islamic Azad University, Gorgan, Iran
4 Department of Morphology, Experimental Medicine and Surgery, Section of Pathology, Oncology and Experimental Biology, University of Ferrara, Ferrara, Italy
5 Department of Medicine, Moores Cancer Center, University of California at San Diego, La Jolla, CA, USA
6 Chronic Lymphocytic Leukemia Research Consortium, San Diego, CA, USA
7 Center for Childhood Cancer & Blood Diseases, The Research Institute at Nationwide Children’s Hospital, Columbus, OH, USA
Correspondence to:
Carlo M. Croce, email:
Keywords: long noncoding RNA MIAT, chronic lymphocytic leukemia, non-Hodgkin’s lymphoma, OCT4, cell apoptosis
Received: May 29, 2016 Accepted: July 14, 2016 Published: August 05, 2016
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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