首页> 外文期刊>International journal of molecular medicine >miR?144?3p inhibits the proliferation, migration and angiogenesis of multiple myeloma cells by targeting myocyte enhancer factor?2A
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miR?144?3p inhibits the proliferation, migration and angiogenesis of multiple myeloma cells by targeting myocyte enhancer factor?2A

机译:mir?144?3p通过靶向肌细胞增强子因子来抑制多发性骨髓瘤细胞的增殖,迁移和血管生成?2a

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Multiple myelomas (MM) are the second most common haematological malignancy, for which no curative treatments have been reported to date. MicroRNAs (miRNAs or miRs) have recently been shown to be involved in the proliferation of MM cells. However, the molecular mechanisms through which miRNAs regulate migration and angiogenesis in MM are poorly understood. Accordingly, the present study evaluated the role of miR?144?3p in MM. miR?144?3p exhibited a lower expression in patients with MM and in MM cell lines compared with normal cells (mononuclear cells derived from bone marrow). The transfection of miR?144?3p into MM cells inhibited proliferation, migration and angiogenesis, and induced cell cycle arrest and apoptosis compared to the control cells. Furthermore, miR?144?3p suppressed the transcription and translation of?the myocyte enhancer factor 2A (MEF2A) gene and disrupted the expression of?vascular endothelial growth factor. The knockdown of MEF2A significantly inhibited the proliferation, migration and angiogenesis of MM cells. However, the overexpression of MEF2A reversed these effects. On the whole, the findings of the present study demonstrate that miR?144?3p exerts antitumour effects by downregulating MEF2A to inhibit the proliferation, migration and angiogenesis of MM cells. This suggests that the miR?144?3p/MEF2A interaction may prove to be a potential therapeutic target for MM.
机译:多个骨髓瘤(mm)是第二种最常见的血液恶性肿瘤,其迄今为止没有报告治疗方法。最近已显示MicroRNA(miRNA或miRs)参与MM细胞的增殖。然而,MiRNA调节MM中的迁移和血管生成的分子机制是较差的。因此,本研究评估了MIR的作用?144?3p以mm。 mir?144?3p与毫米和mm细胞系的患者表现出较低的表达与正常细胞(来自骨髓的单核细胞)。 MiRα144〜3P进入MM细胞的转染抑制了与对照细胞相比的增殖,迁移和血管生成,并诱导细胞周期停滞和凋亡。此外,mir?144?3p抑制了α肌细胞增强子因子2a(mef2a)基因的转录和翻译,并破坏了血管内皮生长因子的表达。 MEF2a的敲低显着抑制MM细胞的增殖,迁移和血管生成。然而,MEF2A的过表达逆转了这些效果。总的来说,本研究的发现表明miR?144?3p通过下调MeF2a抑制MM细胞的增殖,迁移和血管生成来施加抗肿瘤效果。这表明miR?144?3p / mef2a相互作用可以证明是mm的潜在治疗靶标。

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