ArticleAnnals of hematology2026
Clinical value of miR-329-3p in thalassemia and its regulation of TNRC6B expression.
Article in Annals of hematology, 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
Background β-thalassemia is a common monogenic genetic disorder, characterized by reduced or absent synthesis of β-globin chains. High fetal hemoglobin (HbF) levels can alleviate the severity of anemia in β-thalassemia, and miRNAs can regulate the expression of globins. MiR-329-3p is a miRNA that is differentially expressed in β-thalassemia. Aim this study mainly investigated the expression of miR-329-3p in the peripheral blood of children with β-thalassemia, analyzed its clinical diagnostic value in β-thalassemia, and further studied the regulatory effects of miR-329-3p on its target genes TNRC6B and γ-globin. Methods the expression levels of miR-329-3p, TNRC6B, and γ-globin were verified by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). The interaction relationship between miR-329-3 and TNRC6B was confirmed through dual-luciferase assay. Cell viability was detected by the CCK8 method, cell migration rate was verified by Transwell assay, and cell apoptosis rate was determined by cell flow cytometry. Results in children with β-thalassemia, miR-329-3p is upregulated and positively correlates with γ-globin, while TNRC6B is downregulated. MiR-329-3p demonstrates potential diagnostic and prognostic value for β-thalassemia. MiR-329-3p interacts with TNRC6B, and their expression levels show a negative correlation. Knocking down miR-329-3p suppresses the activity and migration of red blood cells, promotes apoptosis, and reduces γ-globin. Conversely, miR-329-3p overexpression enhances red blood cell function, inhibits apoptosis, and increases γ-globin. Conclusions MiR-329-3p has clinical significance in the diagnosis of β-thalassemia. It can inhibit the expression of TNRC6B by upregulation and promote the expression of γ-globin.
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