MiR-218 suppresses metastasis and invasion of endometrial cancer via negatively regulating ADD2
MiR-218 suppresses metastasis and invasion of endometrial cancer via negatively regulating ADD2
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DOI：
10.26355/eurrev_201902_17097
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发表时间：
2019-02-01
影响因子：
3.3
通讯作者：
Liu, L-J
中科院分区：
文献类型：
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作者：
Li, X-C;Hai, J-J;Liu, L-J
目的：子宫内膜癌是妇科三大常见恶性肿瘤之一。由于晚期食管癌患者缺乏有效的治疗手段，食管癌的死亡率迅速上升。因此，寻找新的EC分子治疗靶点和生物标志物是非常必要的。本研究旨在探讨miR-218在EC发生发展中的作用，并探讨其可能的机制。患者与方法：采用定量真实的时间-聚合酶链反应（qRT-PCR）检测miR-218在EC组织和细胞系中的表达水平。伤口愈合实验和Matrigel实验检测EC细胞的迁移和侵袭能力。与此同时通过生物信息学分析预测miR-218的潜在作用靶点，并通过荧光素酶报告基因分析进行验证。结果：QRT-PCR结果显示miR-218在EC组织和细胞系中表达显著下调。伤口愈合实验和Matrigel实验表明miR-218抑制EC细胞的迁移和侵袭能力。在线预测数据库预测ADD 2是miR-218的直接靶点，并通过荧光素酶报告基因检测验证了这一点。拯救实验进一步验证了miR-218可以通过负调控ADD 2在EC.CONCLUSIONS表达作为一个抑癌基因，在本研究中，我们阐明了miR-218作为一个抑癌基因在EC中通过负调控ADD 2。这可能为EC的新分子治疗靶点和生物标志物带来新的见解。
OBJECTIVE: Endometrial cancer (EC) is one of the three most common gynecological cancers. Due to the lack of effective treatment for EC patients in an advanced stage, the mortality rate of EC is increasing rapidly. Hence, it is essential to seek for novel molecular therapeutic targets and biomarkers for EC. The aim of this study was to explore the role of miR-218 in the occurrence and development of EC and to investigate the possible underlying mechanism.PATIENTS AND METHODS: The expression level of miR-218 in EC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Wound healing assay and Matrigel assay were performed to determine the migration and invasion abilities of EC cells. Meanwhile. the potential targets of miR-218 were predicted by bioinformatics analysis and confirmed by Luciferase reporter gene assay. In addition, the protein expression level of Adducin 2 (ADD2) was assessed by Western blotting analysis.RESULTS: QRT-PCR results revealed that miR-218 was significantly downregulated in EC tissues and cell lines. Wound healing assay and Matrigel assay demonstrated that miR-218 suppressed the migration and invasion abilities of EC cells. Online prediction databases predicted that ADD2 was a direct target of miR-218, which was verified by Luciferase reporter gene assay. Rescue experiments further validated that miR-218 could serve as a carcinoma suppressor by negatively regulating ADD2 expression in EC.CONCLUSIONS: In the present study, we elucidated that miR-218 served as a tumor suppressor in EC by negatively regulating ADD2. This might bring a novel insight into new molecular therapeutic targets and biomarkers for EC.