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Effects of microRNA-21 on the biological functions of T-cell acute lymphoblastic lymphoma/leukemia
Author(s) -
Cunzhen Shi,
Xudong Zhang,
Xin Li,
Lei Zhang,
Ling Li,
Zhenchang Sun,
Xiaorui Fu,
Jingjing Wu,
Yu Chang,
Wencai Li,
Qingjiang Chen,
Mingzhi Zhang
Publication year - 2016
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2016.5163
Subject(s) - oncogene , lymphoblastic leukemia , cell cycle , lymphoblastic lymphoma , microrna , molecular medicine , cancer research , lymphoma , medicine , cancer , acute leukemia , leukemia , oncology , biology , immunology , gene , genetics , t cell , immune system
Previous studies have demonstrated that microRNA-21 (miR-21) is an oncogene and is significantly upregulated in tumor tissue. However, its association with T-cell acute lymphoblastic lymphoma/leukemia (T-ALL) remains poorly understood. The aim of the present study was to investigate the effects of miR-21 on T-ALL cells by constructing Jurkat cells infected with recombinant adenovirus adv-miR-21 or adv-anti-miR-21. In addition, the target gene of miR-21 was identified by reverse transcription-quantitative polymerase chain reaction and western blotting. The results demonstrated that miR-21 expression in Jurkat cells was markedly upregulated. Furthermore, upregulating miR-21 expression in Jurkat cells promoted cell proliferation and invasion and decreased the apoptosis rate. By contrast, knockdown of miR-21 in Jurkat cells suppressed proliferation and invasion and increased the apoptosis rate. Furthermore, the results indicated that signal transducer and activator of transcription (STAT) 3 was targeted by miR-21, and that miR-21 inhibited STAT3 expression at the protein level rather than at the messenger RNA level. In conclusion, targeting the inhibition of miR-21 may be a novel therapeutic strategy for patients with T-ALL.

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