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 Blood, 14 May 2009, Vol. 113, No. 20, pp. 4914-4917.
Prepublished online as a Blood First Edition Paper on February 26, 2009; DOI 10.1182/blood-2008-11-189845.

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LYMPHOID NEOPLASIA

Brief Report

Deregulation of microRNA involved in hematopoiesis and the immune response in HTLV-I adult T-cell leukemia

Marcia Bellon1, Yves Lepelletier2, Olivier Hermine2, and Christophe Nicot1

1 University of Kansas Medical Center, Department of Pathology and Laboratory Medicine, Center for Viral Oncology and University of Kansas Cancer Center (KUCC), Kansas City; and 2 Hopital Necker Université Paris V, Centre National de la Recherche Scientifique Unite Mixte de Recherche (CNRS UMR) 8147, Paris, France

Human T-cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult T-cell leukemia (ATL), an aggressive lymphoproliferative disease. MicroRNAs (miRNAs) are differentially expressed during hematopoiesis and lineage commitment of hematopoietic stem cell progenitors (HSCPs). Here, we report aberrant expression of hematopoietic-specific miR-223, miR-181a, miR-150, miR-142.3p, and miR-155 in HTLV-I–infected cells in vitro and uncultured ex vivo ATL cells. Our results suggest that HTLV-I–infected cells have an unbalanced expression of miRNA that favors T-cell differentiation. We also found altered expression of miRNA previously recognized as innate immunity regulators: miR-155, miR-125a, miR-132, and miR-146. Strikingly, our data also revealed significant differences between ex vivo ATL tumor cells and in vitro HTLV-I cell lines. Specifically, miR-150 and miR-223 were up-regulated in ATL patients but consistently down-regulated in HTLV-I cell lines, suggesting that ATL cells and in vitro–established cells are derived from distinct cellular populations.


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