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miR-144-3p inhibits the proliferation, migration and angiogenesis of multiple myeloma cells by targeting myocyte enhancer factor 2A
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 regula...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387096/ https://www.ncbi.nlm.nih.gov/pubmed/32705159 http://dx.doi.org/10.3892/ijmm.2020.4670 |
Sumario: | 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. |
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