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

被引:120
作者
Bellon, Marcia [1 ,2 ]
Lepelletier, Yves [3 ]
Hermine, Olivier [3 ]
Nicot, Christophe [1 ,2 ]
机构
[1] Univ Kansas, Med Ctr, Ctr Viral Oncol, Dept Pathol & Lab Med, Kansas City, KS 66160 USA
[2] Univ Kansas, Ctr Canc, Kansas City, KS 66160 USA
[3] Univ Paris 05, CNRS, Hop Necker, UMR 8147, F-75270 Paris, France
关键词
TRANSCRIPTION FACTOR; HUMAN CANCERS; DIFFERENTIATION; EXPRESSION; REGULATORS; INDUCTION; LYMPHOMA; PROTEINS; TAX;
D O I
10.1182/blood-2008-11-189845
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. (Blood. 2009;113:4914-4917)
引用
收藏
页码:4914 / 4917
页数:4
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