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首页> 外文期刊>Cellular Physiology and Biochemistry >MiR-424 Promotes Non-Small Cell Lung Cancer Progression and Metastasis through Regulating the Tumor Suppressor Gene TNFAIP1
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MiR-424 Promotes Non-Small Cell Lung Cancer Progression and Metastasis through Regulating the Tumor Suppressor Gene TNFAIP1

机译：MiR-424通过调节肿瘤抑制基因TNFAIP1促进非小细胞肺癌的进展和转移。

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>Background/Aims: This study aimed to investigate the potential roles of miR-424 expression in non-small cell lung cancer (NSCLC) metastasis and growth and its underlying mechanism. Methods: The expression of miR-424 in two NSCLC cell lines (A549 and H1975) was altered by transfection with miR-424 mimic and inhibitor. Effects of miR-424 overexpression and suppression on cells migration, invasion and colony formation were analyzed. Target genes for miR-424 were predicted using bioinformatics method and then verified using luciferase assay. Effects of miR-424 expression on cell migration, invasion and proliferation were reanalyzed on the condition of TNFAIP1 was silenced. Moreover, TNFAIP1 silencing and miR-424 modified A549 cells were subcutaneous injected into node BALB/c mice to confirm the regulation of miR-424 on TNFAIP1 in regulating tumor growth. Results: Compared with the control, miR-424 overexpression significantly increased the migrated and invaded cells, as well as the proliferated colonies. TNFAIP1 was a predicted target gene for miR-424, and was negatively regulated by miR-424. TNFAIP1 silence significantly increased the migrated and invaded cells compared to that in control, while these increases were abolished by miR-424 suppression. Animal experiment further evidenced miR-424 affected tumor growth by regulating TNFAIP1. Conclusions: These data demonstrate that miR-424 may be a contributor for NSCLC progression and metastasis through involving in cell migration, invasion and proliferation via inhibiting TNFAIP1. This study may provide theoretical basis for miR-424 in NSCLC target therapeutic treatment.
机译：> 背景/目的： 这项研究旨在研究miR-424表达在非小细胞肺癌（NSCLC）转移和生长中的潜在作用及其潜在意义机制。 方法： 用miR-424模拟物和抑制剂转染可改变miR-424在两种NSCLC细胞系（A549和H1975）中的表达。分析了miR-424过表达和抑制对细胞迁移，侵袭和集落形成的影响。使用生物信息学方法预测miR-424的靶基因，然后使用萤光素酶测定法对其进行验证。在沉默TNFAIP1的条件下，重新分析了miR-424表达对细胞迁移，侵袭和增殖的影响。此外，将TNFAIP1沉默和miR-424修饰的A549细胞皮下注射到结节BALB / c小鼠中，以证实miR-424对TNFAIP1的调节对肿瘤生长的调节。 结果： 与对照组相比，miR-424过表达显着增加了迁移和侵袭的细胞以及增殖的菌落。 TNFAIP1是miR-424的预期靶基因，并受miR-424负调控。与对照相比，TNFAIP1沉默显着增加了迁移和侵袭的细胞，而miR-424抑制则消除了这些增加。动物实验进一步证明miR-424通过调节TNFAIP1影响肿瘤的生长。 结论： 这些数据表明，miR-424可能通过抑制TNFAIP1参与细胞迁移，侵袭和增殖，从而成为NSCLC进展和转移的原因。该研究可为miR-424在NSCLC靶标治疗中的应用提供理论依据。

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