microRNA-22 can regulate expression of the long non-coding RNA MEG3 in acute myeloid leukemia
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Hongxia Yao1,*, Pei Sun2,*, Mengling Duan1,*, Lie Lin1, Yanping Pan1, Congming Wu1, Xiangjun Fu1, Hua Wang1, Li Guo1, Tianbo Jin3 and Yipeng Ding4
1Department of Hematology, Hainan General Hospital, Haikou, Hainan 570311, P.R. China
2Department of Hematology, Hunan Yiyang Central Hospital, Yiyang, Hunan 413000, P.R. China
3Key Laboratory of Resource Biology and Biotechnology in Western China (Northwest University), Ministry of Education, Xi’an, Shaanxi 710069, P.R. China
4Department of Emergency, Hainan General Hospital, Haikou, Hainan 570311, P.R. China
*These authors have contributed equally to this work
Hongxia Yao, email: [email protected]
Yipeng Ding, email: [email protected]
Keywords: acute myeloid leukemia(AML), MEG3, long non-coding RNA, TET2, miR-22-3p/5p
Received: March 22, 2017 Accepted: April 19, 2017 Published: May 22, 2017
Aim: Acute myeloid leukemia (AML) is the most common blood tumor with poor prognosis. At present, the research found that the pathogenesis of AML is related to many factors, such as recurrent somatic mutations and gene expression and epigenetic changes, however, the molecular mechanism of AML is still unclear. Long non-coding RNA MEG3 is a newly found tumor suppressor and plays a very important role in the regulation of a variety of tumor formation and progression. Studies found that the MEG3 expression was significantly decreased in AML. However, to date, it is not clear the cause of its abnormal expression. Therefore, the molecular mechanism of AML is urgently needed to study the molecular mechanism of AML.
Methods: The different expression level of MEG3, TET2, miR-22-3p, miR-22-5p in AML was detected by real-time quantification PCR. MEG3, TET2, miR-22-3p, miR-22-3p expression cell pools in K562 cells was used to interfering and TET2, MEG3 TET2, relations with miR-22-3p, miR-22-5p. The effect of AML cell on proliferation was evaluated by TET2 lower expression.
Results: 1. The lower expression of MEG3 and TET2 in AML cell lines was detected by RT-qPCR. 2. The stable MEG3, TET2 overexpression cell pools in K562 cells was successful established. 3. After transfection, MTT assay revealed that cell growth was significantly increased in AML cell lines transfected with TET2 compared with controls.
Conclusions: Our findings suggested that MEG3 is significantly down regulated in AML cell lines.
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