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The Effect of MEG3 Promoter Methylation on MEG3 Expression in Acute Myeloid Leukemia: Assessment by High-Resolution
Ali Asgharzadeh1, Alireza Moradabadi2,3,4, Ali Noroozi-Aghideh1
1Department of Hematology, Faculty of Allied Medical Sciences, AJA University of Medical Sciences, Tehran, Iran.
Introduction:
Epigenetic mechanisms play a crucial role in regulating genome expression and are subject to dysregulation in leukemia, hence exerting a significant impact on the pathogenesis of this malignancy. Maternally expressed gene 3 (MEG3), a long non-coding RNA, has been identified as a tumor suppressor in many hematologic malignancies due to its frequent down-regulation. This study aimed to examine the expression and methylation status of MEG3 in patients diagnosed with acute myeloid leukemia by employing the High-Resolution Melting (HRM) method.
Materials And Methods:
The study employed quantitative RT-PCR to assess the expression of MEG3 in peripheral blood mononuclear cells (PBMCs) derived from a cohort of 62 individuals diagnosed with AML and 32 individuals as healthy controls. The study used the methylation-sensitive high-resolution melting (MS-HRM) method to assess the methylation status of the MEG3 promoter region.
Results:
The MEG3 expression was significantly downregulated (P <0.0001) in patients with AML compared to healthy controls. Furthermore, the methylation level of the MEG3 promoter was significantly different between patients and controls (P<0.001). The average methylation rate of the MEG3 gene promoter in patients was 70.3%. A statistically significant negative association (r = -0.32, p = 0.03) was observed between MEG3 methylation and its expression.
Discussion:
The expression of the MEG3 gene exhibited a significant decrease, while the promoter methylation level was elevated in patients. These findings suggest that MEG3 may function as a tumor suppressor gene and may have potential as a prognostic biomarker in AML. These findings suggest that targeting aberrant MEG3 promoter methylation could represent a potential therapeutic strategy in AML, though further studies are warranted to confirm this hypothesis.
