TET2 and MEG3 promoter methylation is associated with acute myeloid leukemia in a Hainan population
Metrics: PDF 1181 views | HTML 1433 views | ?
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
Hongxia Yao, email: email@example.com
Keywords: AML, Hainan, LncRNA MEG3, TET2, rtPCR
Received: December 02, 2016 Accepted: January 11, 2017 Published: February 17, 2017
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.