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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 &lt; 0.05). Methylation of the MEG3 promoter correlated negatively with TET2 expression (P &lt; 0.05, r &lt; 0). Likewise there was a negative correlation between TET2 activity and MEG3 promoter methylation (P &lt; 0.05, r &lt; 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.

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