ArticleJournal of blood medicine2026
The Effect of MEG3 Promoter Methylation on MEG3 Expression in Acute Myeloid Leukemia: Assessment by High-Resolution Melting (HRM) Analysis.
Article in Journal of blood medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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