微小RNA-410通过靶向BRD7促进非小细胞肺癌细胞增殖。
MicroRNA-410 promotes cell proliferation by targeting BRD7 in non-small cell lung cancer.
作者信息
Li Dengrui, Yang YongHui, Zhu GuiYun, Liu XinYan, Zhao Min, Li XiaoXia, Yang QinOu
机构信息
Department of General Internal Medicine, Chest Hospital of Hebei Province, Shijiazhuang, Hebei 050041, China.
Department of Pathology, Chest Hospital of Hebei Province, Shijiazhuang, Hebei 050041, China.
出版信息
FEBS Lett. 2015 Aug 4;589(17):2218-23. doi: 10.1016/j.febslet.2015.06.031. Epub 2015 Jul 3.
miR-410 acts as an oncogene or tumor suppressor gene in some malignancies. However, its role in NSCLC is still unknown. In this study, we showed that the expression of miR-410 was up-regulated in both human NSCLC tissues and cells. Overexpression of miR-410 promoted cell proliferation, migration, and invasion of NSCLC. In addition, bromodomain-containing protein 7 (BRD7) was a direct target of miR-410. MiR-410-mediated downregulation of BRD7 led to increase Akt phosphorylation. Inhibition of Akt phosphorylation can rescue the effect of miR-410 on NSCLC cell. The expression of BRD7 was downregulated in NSCLC and was inversely expressed with miR-410 in NSCLC. Our data provided new knowledge regarding the role of miR-410 in the lung cancer progression.
在某些恶性肿瘤中，miR-410可作为癌基因或肿瘤抑制基因。然而，其在非小细胞肺癌（NSCLC）中的作用仍不清楚。在本研究中，我们发现miR-410在人NSCLC组织和细胞中表达均上调。miR-410的过表达促进了NSCLC细胞的增殖、迁移和侵袭。此外，含溴结构域蛋白7（BRD7）是miR-410的直接靶点。miR-410介导的BRD7下调导致Akt磷酸化增加。抑制Akt磷酸化可挽救miR-410对NSCLC细胞的作用。BRD7在NSCLC中表达下调，且与NSCLC中的miR-410呈负相关表达。我们的数据为miR-410在肺癌进展中的作用提供了新的认识。
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