Oncotarget

Research Papers:

TET2 and MEG3 promoter methylation is associated with acute myeloid leukemia in a Hainan population

Hongxia Yao _, Mengling Duan, Lie Lin, Congming Wu, Xiangjun Fu, Hua Wang, Li Guo, Wenting Chen, Li Huang, Dan Liu, Ruo Rao, Shuwen Wang and Yipeng Ding

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Oncotarget. 2017; 8:18337-18347. https://doi.org/10.18632/oncotarget.15440

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Abstract

Hongxia Yao1,*, Mengling Duan1,*, Lie Lin1, Congming Wu1, Xiangjun Fu1, Hua Wang1, Li Guo1, Wenting Chen1, Li Huang1, Dan Liu1, Ruo Rao1, Shuwen Wang1, Yipeng Ding2

1Department of Hematology, Hainan General Hospital, Haikou, Hainan, 570311, P.R. China

2Department of Emergency, Hainan General Hospital, Haikou, Hainan, 570311, P.R. China

*These authors have contributed equally to this work

Correspondence to:

Hongxia Yao, email: yaohongxiahk@163.com

Keywords: AML, Hainan, LncRNA MEG3, TET2, rtPCR

Received: December 02, 2016     Accepted: January 11, 2017     Published: February 17, 2017

ABSTRACT

The promoter of MEG3, which encodes the long non-coding RNA (lncRNA) MEG3, is often hypermethylated in acute myeloid leukemia (AML). Additionally, the Tet methylcytosine dioxygenase 2 gene (TET2) is frequently inactivated, which can lead to impaired DNA methylation and promote AML development. We examined the association between TET2 and MEG3 promoter hypermethylation in Hainan patients with AML. The expression of MEG3, TET2, miR-22-3p, and miR-22-5p was assessed in bone marrow samples from AML patients and healthy controls using real-time quantitative PCR. Using Sequenom MassARRAY technology, we compared MEG3 promoter methylation in AML patients and healthy controls. MEG3 expression was lower in AML patients than in the controls (P = 0.136). Moreover, there was greater methylation of MEG3 promoter in the AML patients than the controls (P < 0.05). Methylation of the MEG3 promoter correlated negatively with TET2 expression (P < 0.05, r < 0). Likewise there was a negative correlation between TET2 activity and MEG3 promoter methylation (P < 0.05, r < 0). These results suggest that hypermethylation of the MEG3 promoter in AML may result from decreased TET2 activity. These data provide insight into the molecular mechanisms underlying AML development and progression.


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