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BioMed Research International
Volume 2015, Article ID 197241, 10 pages
Research Article

MicroRNA181a Is Overexpressed in T-Cell Leukemia/Lymphoma and Related to Chemoresistance

1State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Shanghai Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China
2French-Chinese Laboratory of Genomic and Life Sciences, Laboratory of Molecular Pathology, Shanghai 200025, China
3Department of Hematology, Central Hospital of Jinhua, Zhejiang 321000, China
4Department of Pathology, Shanghai Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China
5Department of Oncology, People’s Hospital of Guizhou Province, Guiyang 550001, China
6Laboratory of Pathology, Paris Diderot University, U1165 Inserm, 75010 Paris, France

Received 16 October 2014; Revised 20 January 2015; Accepted 27 January 2015

Academic Editor: Jin Wang

Copyright © 2015 Zi-Xun Yan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


MicroRNAs (miRs) play an important role in tumorogenesis and chemoresistance in lymphoid malignancies. Comparing with reactive hyperplasia, miR181a was overexpressed in 130 patients with T-cell leukemia/lymphoma, including acute T-cell lymphoblastic leukemia (), T-cell lymphoblastic lymphoma (), peripheral T-cell lymphoma, not otherwise specified (), anaplastic large cell lymphoma (), and angioimmunoblastic T-cell lymphoma (). Irrespective to histological subtypes, miR181a overexpression was associated with increased AKT phosphorylation. In vitro, ectopic expression of miR181a in HEK-293T cells significantly enhanced cell proliferation, activated AKT, and conferred cell resistance to doxorubicin. Meanwhile, miR181a expression was upregulated in Jurkat cells, along with AKT activation, during exposure to chemotherapeutic agents regularly applied to T-cell leukemia/lymphoma treatment, such as doxorubicin, cyclophosphamide, cytarabine, and cisplatin. Isogenic doxorubicin-resistant Jurkat and H9 cells were subsequently developed, which also presented with miR181a overexpression and cross-resistance to cyclophosphamide and cisplatin. Meanwhile, specific inhibition of miR181a enhanced Jurkat and H9 cell sensitivity to chemotherapeutic agents, further indicating that miR181a was involved in acquired chemoresistance. Collectively, miR181a functioned as a biomarker of T-cell leukemia/lymphoma through modulation of AKT pathway. Related to tumor cell chemoresistance, miR181a could be a potential therapeutic target in treating T-cell malignancies.