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首页> 外文期刊>Cellular Physiology and Biochemistry >MicroRNA-29a Inhibits Growth, Migration and Invasion of Melanoma A375 Cells in Vitro by Directly Targeting BMI1
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MicroRNA-29a Inhibits Growth, Migration and Invasion of Melanoma A375 Cells in Vitro by Directly Targeting BMI1

机译：通过直接靶向BMI1 MicroRNA-29a抑制黑素瘤A375细胞的生长，迁移和侵袭。

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Background/Aims Melanoma is one of the most aggressive malignant tumors, with increasing incidence, poor prognosis, and lack of any effective targeted therapies. Abnormal expression of miR-29a has been found in several types of cancers, including melanoma. In this study, experiments were performed to investigate the role of miR-29a in melanoma, and the molecular mechanism by which miR-29a represses melanoma. Methods miR-29 and Bmi1 expression was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability, apoptosis, migration and invasion were respectively determined by Cell Counting Kit-8 assay, Propidium iodide (PI) fluorescein isothiocynate (FITC)-Annexin V staining assay, wound healing assay and transwell assay. Luciferase reporter assay was performed to determine a target gene of miR-29a. Western blot was used to analyze protein expression of apoptosis-related proteins, Bmi1, Wnt/β-catenin and Nuclear factor-κB (NF-κB) pathway target genes. Results miR-29a was down-regulated in all tested melanoma cell lines. Up-regulation of miR-29a effectively inhibited cell viability, migration, and invasion, but promoted apoptosis in A375 cells. Bmi1 was a direct target gene of miR-29a. Transfection with miR-29a mimic decreased cell migration and invasion and Bmi1 expression in Malme-3M cells, SK-MEL-2, SK-MEL-5, and M14 cell lines. Moreover, miR-29a might suppress growth, migration and invasion of A375 cells by negatively regulating Bmi1. In addition, our results demonstrated that transfection with miR-29a mimic effectively blocked Wnt/β-catenin and NF-κB pathways via down-regulating Bmi1. Conclusion miR-29a could be functioned as a potential tumor suppressor through direct regulation of Bmi1 in melanoma cells.
机译：背景/目的黑色素瘤是最具有侵略性的恶性肿瘤之一，其发病率不断增加，预后不良且缺乏任何有效的靶向治疗方法。在包括黑素瘤在内的几种类型的癌症中发现了miR-29a的异常表达。在这项研究中，进行了实验以研究miR-29a在黑色素瘤中的作用，以及miR-29a抑制黑色素瘤的分子机制。方法采用定量实时聚合酶链反应（qRT-PCR）检测miR-29和Bmi1的表达。细胞活力，凋亡，迁移和侵袭分别通过Cell Counting Kit-8测定，碘化丙啶（PI）异硫氰酸荧光素（FITC）-Annexin V染色测定，伤口愈合测定和transwell测定来确定。进行荧光素酶报告基因测定以确定miR-29a的靶基因。 Western blot分析细胞凋亡相关蛋白，Bmi1，Wnt /β-catenin和NF-κB（NF-κB）途径靶基因的表达。结果在所有测试的黑色素瘤细胞系中miR-29a均下调。 miR-29a的上调有效抑制细胞活力，迁移和侵袭，但促进A375细胞凋亡。 Bmi1是miR-29a的直接靶基因。用miR-29a模拟转染可减少Malme-3M细胞，SK-MEL-2，SK-MEL-5和M14细胞系中的细胞迁移和侵袭以及Bmi1表达。而且，miR-29a可能通过负调节Bmi1抑制A375细胞的生长，迁移和侵袭。此外，我们的研究结果表明，miR-29a模拟转染可通过下调Bmi1有效地阻断Wnt /β-catenin和NF-κB通路。结论miR-29a可能通过直接调节黑色素瘤细胞中的Bmi1发挥潜在的抑癌作用。

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