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首页> 外文期刊>Thoracic cancer. >Transcriptional factor FOXO3 negatively regulates the expression of nm23‐H1 in non‐small cell lung cancer
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Transcriptional factor FOXO3 negatively regulates the expression of nm23‐H1 in non‐small cell lung cancer

机译：转录因子FOXO3负调节非小细胞肺癌中nm23-H1的表达

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AbstractBackground: Nm23-H1 was the first metastasis suppressor discovered in most tumor models and reduction or loss of nm23-H1 expression correlates with tumor progression and metastasis in non-small-cell lung cancer. Despite extensive studies, the regulatory mechanism of nm23-H1 expression is far from elucidated. The transcriptional factor forkhead box (FOX)O3 has been reported to be involved in multiple regulatory signaling pathways in the biological behavior of tumors. Therefore, we aimed to study the relationship between FOXO3 activity and nm23-H1 expression.Methods: Real time reverse transcriptase-polymerase chain reaction and Western blotting assays were employed to determine nm23-H1 messenger ribonucleic acid and protein expression after being transformed by different FOXO3 plasmid in A549 cells. A dual luciferase reporter system and chromatin immunoprecipitation assay, were used to determine the promoter activity of the nm23-H1 gene and to detect the binding of FOXO3 into the nm23-H1 promoter, respectively.Results: We found that activated FOXO3 decreased nm23-H1 expression and dominant negative FOXO3 increased nm23-H1 expression. Modulation of FOXO3 activity with FOXO3 pathway inhibitors altered nm23-H1 promoter activity. Although there is a putative binding site of FOXO3 in the nm23-H1 promoter, FOXO3 regulated nm23-H1 expression in an indirect manner.Conclusion: We demonstrated that the transcriptional factor FOXO3 decreased the expression levels of the tumor suppressor gene nm23-H1 in the non-small-cell lung cancer A549 cell line and that the level of expression of nm23-H1 was controlled by FOXO3 in an indirect manner. This finding provided an insight into the upstream regulation of nm23-H1 and may provide promising targets for inhibition of the metastasis process.
机译：摘要背景：Nm23-H1是在大多数肿瘤模型中发现的第一个转移抑制因子，nm23-H1表达的减少或丧失与非小细胞肺癌的肿瘤进展和转移相关。尽管进行了广泛的研究，但仍未阐明nm23-H1表达的调控机制。据报道，转录因子叉头盒（FOX）O3参与了肿瘤生物学行为中的多个调控信号通路。因此，我们旨在研究FOXO3活性与nm23-H1表达之间的关系。方法：采用实时逆转录聚合酶链反应和Western blotting方法，分别测定经不同FOXO3转化的nm23-H1信使核糖核酸和蛋白质表达。 A549细胞中的质粒。结果：found我们发现活化的FOXO3降低了nm23-H1的启动子活性，并检测了FOXO3与nm23-H1的启动子的结合。表达和显性负FOXO3增加nm23-H1表达。用FOXO3途径抑制剂调节FOXO3活性改变了nm23-H1启动子活性。尽管在nm23-H1启动子中有一个可能的FOXO3结合位点，但FOXO3间接调节了nm23-H1的表达。结论：我们证明了转录因子FOXO3降低了抑癌基因nm23-H1在肿瘤中的表达水平。非小细胞肺癌A549细胞株和nm23-H1的表达水平由FOXO3间接控制。该发现提供了对nm23-H1的上游调节的见解，并且可以为抑制转移过程提供有希望的靶标。

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