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Author Xue, Wen ♦ Huang, Li-Min ♦ Zhao, Wei-Li ♦ Janin, Anne ♦ Wang, Li ♦ Zhao, Ming-Zhe ♦ Yan, Zi-Xun ♦ Leboeuf, Christophe ♦ Fei, Xiao-Chun ♦ Wu, Li-Li ♦ Zheng, Zhong
Source Directory of Open Access Journals (DOAJ)
Content type Text
Publisher Hindawi Limited
File Format HTM / HTML
Date Created 2015-09-20
Copyright Year ©2015
Language English
Subject Domain (in LCC) R
Subject Keyword Medicine
Abstract 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 (n=32), T-cell lymphoblastic lymphoma (n=16), peripheral T-cell lymphoma, not otherwise specified (n=45), anaplastic large cell lymphoma (n=15), and angioimmunoblastic T-cell lymphoma (n=22). 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.
ISSN 23146133
Age Range 18 to 22 years ♦ above 22 year
Educational Use Research
Education Level UG and PG ♦ Career/Technical Study
Learning Resource Type Article
Publisher Date 2015-01-01
e-ISSN 23146133
Journal BioMed Research International
Volume Number 2015


Source: Directory of Open Access Journals (DOAJ)