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首页> 外文期刊>Cell biology international. >MiR‐9 promotes multiple myeloma progression by regulating TRIM56/NF‐κB pathway
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MiR‐9 promotes multiple myeloma progression by regulating TRIM56/NF‐κB pathway

机译：miR-9通过调节Trim56 / NF-κB途径来促进多种骨髓瘤进展

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Abstract miR‐9 has been reported to play a pivotal role in multiple human cancers by acting as an oncogene or tumor suppressor. In this study, we explored the possible role and molecular mechanism of miR‐9 in multiple myeloma (MM). The miR‐9 expression was examined by quantitative real‐time polymerase chain reaction assay. Transfection with miR‐9‐mimics, miR‐9‐inhibitor, pcDNA‐TRIM56, or si‐TRIM56 into cells was used to change the expression levels of miR‐9 and TRIM56. Western blot analysis was used to detect the expression of TRIM56, p65, p‐p65, IκBα, and p‐IκBα. The potential target of miR‐9 was confirmed by luciferase reporter assay. The 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium (MTT) assay, colony formation assay, and flow cytometry were used to assess the abilities of cell proliferation and apoptosis. miR‐9 was upregulated in MM patients and cell lines, and miR‐9 overexpression promoted proliferation and repressed apoptosis in MM cell lines. TRIM56 was confirmed as a target of miR‐9. Moreover, TRIM56 reversed miR‐9‐mediated pro‐proliferation and anti‐apoptosis effect on MM cell lines. Furthermore, nuclear factor‐κB (NF‐κB) pathway was involved in miR‐9/TRIM56‐mediated regulation on MM cell lines. miR‐9 promoted the development and progression of MM by regulating TRIM56/NF‐κB pathway, thereby providing a potential microRNA‐based target for MM therapy.
机译：据报道，摘要MIR-9通过作为癌基因或肿瘤抑制剂来发挥多种人类癌症的枢轴作用。在这项研究中，我们探讨了多发性骨髓瘤（mm）中miR-9的可能作用和分子机制。通过定量实时聚合酶链反应测定检查MIR-9表达。使用miR-9 - 模拟物，miR-9抑制剂，pcdna-tem56或Si-trim56转染在细胞中，改变miR-9和Trim56的表达水平。 Western印迹分析用于检测Trim56，P65，P-P65，IκBα和P-IκBα的表达。通过荧光素酶报告器测定证实miR-9的潜在靶标。使用3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑鎓（MTT）测定，菌落形成测定和流式细胞术来评估细胞增殖和细胞凋亡的能力。 MIR-9在MM患者和细胞系中上调，MIR-9过表达促进MM细胞系中的增殖和压抑凋亡。 Trim56被证实为miR-9的靶标。此外，TRIM56反转MIR-9介导的促进和抗凋亡作用对MM细胞系。此外，核因子-κB（NF-κB）途径参与MIR-9 / TRIM56介导的MM细胞系调控。 MiR-9通过调节Trim56 / NF-κB途径促进MM的开发和进展，从而提供潜在的MICRNA靶标进行MM疗法。

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