Here, we aimed to investigate the biological roles and the regulatory mechanisms of miR-335-3p in acute myeloid leukemia (AML). We first found miR-335-3p was significantly downregulated in blood samples from leukemia patients and cell lines using reverse transcription quantitative polymerase chain reaction. Through CCK-8 assay and flow cytometry, we observed that miR-335-3p overexpression significantly inhibited cell proliferation and induced cell cycle G0/G1 arrest and apoptosis in AML cell lines (THP-1 and U937). Moreover, miR-335-3p directly targets EIF3E and negatively regulated its expression. More importantly, EIF3E overexpression reversed the effects of miR-335-3p on cell proliferation, G1/S transition, and apoptosis. Furthermore, miR-335-3p overexpression obviously downregulated the expression of CDK4, Cyclin D1, and Bcl-2, while upregulated the expression of p21 and Bad, which were significantly rescued by the cotransfection of pcDNA3.1-EIF3E. Collectively, our study proposes that miR-335-3p/EIF3E axis could be a promising therapeutic target to mitigate the progression of AML.

中文翻译：

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MiR-335-3p 通过靶向 EIF3E 在急性髓性白血病中抑制细胞增殖并诱导细胞周期停滞和凋亡。

在这里，我们旨在研究 miR-335-3p 在急性髓性白血病 (AML) 中的生物学作用和调控机制。我们首先使用逆转录定量聚合酶链反应发现 miR-335-3p 在白血病患者的血液样本和细胞系中显着下调。通过 CCK-8 测定和流式细胞术，我们观察到 miR-335-3p 过表达显着抑制 AML 细胞系（THP-1 和 U937）的细胞增殖并诱导细胞周期 G0/G1 期阻滞和凋亡。此外，miR-335-3p 直接靶向 EIF3E 并负调控其表达。更重要的是，EIF3E 过表达逆转了 miR-335-3p 对细胞增殖、G1/S 转变和细胞凋亡的影响。此外，miR-335-3p 过表达明显下调 CDK4、Cyclin D1 和 Bcl-2 的表达，同时上调 p21 和 Bad 的表达，通过共转染 pcDNA3.1-EIF3E 显着挽救了 p21 和 Bad 的表达。总的来说，我们的研究表明 miR-335-3p/EIF3E 轴可能是缓解 AML 进展的有希望的治疗靶点。