miR-196b inhibits cell migration and invasion through targeting MAP3K1 in hydatidiform mole
miR-196b inhibits cell migration and invasion through targeting MAP3K1 in hydatidiform mole
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miR-196b 通过靶向葡萄胎中的 MAP3K1 抑制细胞迁移和侵袭。
DOI：
10.1016/j.biopha.2019.108760
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发表时间：
2019-05-01
影响因子：
7.5
通讯作者：
Kong，Ying
中科院分区：
文献类型：
--
作者：
Guo，Zhenzhen;Sui，Linlin;Kong，Ying
microRNAs（miRNAs）是一类与肿瘤发生密切相关的小分子非编码RNA。越来越多的数据表明，miR-196 b参与了各种类型癌症的发展。然而，miR-196 b在葡萄胎（HM）形成中的作用仍不清楚。我们先前的研究已经证明，miR-196 b水平在ESTO和BeWo细胞以及HM组织样品中降低，如通过RT-PCR分析所证明的。此外，我们发现miR-196 b在BMSCs和BeWo细胞中的过表达抑制细胞增殖、迁移和侵袭，如分别通过细胞计数试剂盒-8（CCK-8）和transwell测定所示。随后，我们探讨了miR-196 b与其靶基因在人绒毛膜癌细胞系中的相互作用。MAP 3 K1是通过生物信息学分析预测的靶基因，其先前显示在用miR-196 b处理后在BEC和BeWo细胞中表现出降低的表达水平。我们在Hela细胞中使用双荧光素酶报告基因测定证明了MAP 3 K1是miR-196 b的直接靶点。综上所述，本研究证实miR-196 b通过抑制其转录靶点MAP 3 K1抑制人绒毛膜癌细胞的增殖、迁移和侵袭。miR-196 b和MAP 3 K1可能被认为是HM临床治疗的潜在靶点。
MicroRNAs (miRNAs) are a class of small non-coding RNAs that are closely associated with carcinogenesis. Accumulating data indicate that miR-196b participates in the development of various types of cancers. However, the role of miR-196b in the formation of hydatidiform mole (HM) is still unclear. Our previous studies have demonstrated that miR-196b levels were decreased in JAR and BeWo cells and in HM tissue samples, as demonstrated by RT-PCR analysis. Furthermore, we discovered that overexpression of miR-196b in JAR and BeWo cells inhibited cellular proliferation, migration and invasion, as shown by Cell counting kit-8 (CCK-8) and transwell assays, respectively. Subsequently, we explored the interaction of miR-196b with its target gene in human choriocarcinoma cell lines. MAP3K1 is a target gene predicted by bioinformatic analysis that was previously shown to exhibit reduced expression levels following treatment with miR-196b in JAR and BeWo cells. We demonstrated that MAP3K1 was a direct target of miR-196b using the dual-luciferase reporter assay in Hela cells. In summary, the present study demonstrated that miR-196b suppressed proliferation, migration and invasion of human choriocarcinoma cells by inhibiting its transcriptional targetMAP3K1. miR-196b and MAP3K1 may be considered potential targets for the clinical treatment of HM.