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Journal of Virology, December 2009, p. 12009-12017, Vol. 83, No. 23
0022-538X/09/$08.00+0     doi:10.1128/JVI.01182-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Reticuloendotheliosis Virus Strain T Induces miR-155, Which Targets JARID2 and Promotes Cell Survival {triangledown}

Mohan T. Bolisetty,1 George Dy,1 Wayne Tam,2 and Karen L. Beemon1*

Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218,1 Department of Pathology and Laboratory Medicine, The Joan and Sanford I. Weill Medical College of Cornell University, New York, New York 100212

Received 9 June 2009/ Accepted 7 September 2009

The oncogenic microRNA miR-155 is upregulated by several oncogenic viruses. The precursor of miR-155, termed bic, was first observed to cooperate with myc in chicken B-cell lymphomas induced by avian leukosis proviral integrations. We identified another oncogenic retrovirus, reticuloendotheliosis virus strain T (REV-T), that upregulates miR-155 in chicken embryo fibroblasts. We also observed very high levels of miR-155 in REV-T-induced B-cell lymphomas. To study the role of miR-155 in these tumors, we identified JARID2/Jumonji, a cell cycle regulator and part of a histone methyltransferase complex, as a target of miR-155. The overexpression of miR-155 decreased levels of endogenous JARID2 mRNA. We confirmed that miR-155 directly targets both human and chicken JARID2 by assaying the repression of reporters containing the JARID2 3'-untranslated regions. Further, the overexpression of a sponge complementary to miR-155 in a tumor cell line increased endogenous JARID2 mRNA levels. The overexpression of JARID2 in chicken fibroblasts led to decreased cell numbers and an increase in apoptotic cells. The overexpression of miR-155 rescued cells undergoing cytopathic effect caused by infection with subgroup B avian retroviruses. Therefore, we propose that miR-155 has a prosurvival function that is mediated through the downregulation of targets including JARID2.

* Corresponding author. Mailing address: Biology Department, Johns Hopkins University, 3400 N Charles Street, Baltimore, MD, 21218. Phone: (410) 516-7289. Fax: (410) 516-7292. E-mail: KLB{at}jhu.edu

{triangledown} Published ahead of print on 16 September 2009.

Journal of Virology, December 2009, p. 12009-12017, Vol. 83, No. 23
0022-538X/09/$08.00+0     doi:10.1128/JVI.01182-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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