MicroRNA-6884-5p Regulates the Proliferation, Invasion, and EMT of Gastric Cancer Cells by Directly Targeting S100A16.
MicroRNA-6884-5p Regulates the Proliferation, Invasion, and EMT of Gastric Cancer Cells by Directly Targeting S100A16.
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DOI：
10.3727/096504019x15753718797664
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发表时间：
2020-05-29
影响因子：
3.1
通讯作者：
Chen X
中科院分区：
文献类型：
--
作者：
Lv H;Hou H;Lei H;Nie C;Chen B;Bie L;Han L;Chen X
S100 结合蛋白 A16 (S100A16) 表达水平与 microRNA (miRNA) 加工密切相关。据报道，在许多癌症的进展过程中，S100A16 的水平会升高。我们的研究主要探讨了 S100A16 和 miR-6884-5p 在胃癌（GC）中的相互作用。采用实时定量聚合酶链反应（qRT-PCR）测定GC组织和细胞系中S100A16和miR-6884-5p的水平。将si-S100A16、pcDNA-S100A16、miR-6884-5p模拟物或抑制剂转染到GC细胞中，通过qRT-PCR和Western blot分析探讨S100A16和miR-6884-5p对增殖、侵袭和上皮间质转化（EMT）的影响。进行荧光素酶测定以验证 S100A16 作为 GC 细胞中的 miR-6884-5p 靶标。在我们的研究中，我们发现GC组织和细胞系中miR-6884-5p的水平显着降低，S100A16的表达显着增加。这些变化之间有着密切的联系。 S100A16的敲低显着抑制GC细胞的增殖、侵袭和EMT。生物信息学分析预测S100A16是miR-6884-5p的潜在靶基因，荧光素酶报告基因检测证实miR-6884-5p可以直接靶向S100A16。将 miR-6884-5p 引入 GC 细胞具有与 S100A16 沉默相似的效果。 GC 细胞中 S100A16 的过度表达部分逆转了 miR-6884-5p 模拟物的抑制作用。 miR-6884-5p通过直接降低S100A16的表达来抑制GC细胞的增殖、侵袭和EMT。
S100 binding protein A16 (S100A16) expression levels are closely associated with microRNA (miRNA) processing. Higher levels of S100A16 are reported during the progression of many cancers. Our study mainly explored the interaction between S100A16 and miR-6884-5p in gastric cancer (GC). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the level of S100A16 and miR-6884-5p in GC tissues and cell lines. The si-S100A16, pcDNA-S100A16, miR-6884-5p mimic or inhibitor was transfected into GC cells, and the effects of S100A16 and miR-6884-5p on the proliferation, invasion, and epithelial–mesenchymal transition (EMT) were explored by qRT-PCR and Western blot assays. Luciferase assays were performed to validate S100A16 as an miR-6884-5p target in GC cells. In our study, we found that the level of miR-6884-5p was significantly decreased and the expression of S100A16 was significantly increased in GC tissues and cell lines. There was a close association between these changes. Knockdown of S100A16 significantly inhibited the proliferation, invasion, and EMT of GC cells. The bioinformatics analysis predicted that S100A16 is a potential target gene of miR-6884-5p, and the luciferase reporter assay confirmed that miR-6884-5p could directly target S100A16. Introduction of miR-6884-5p to GC cells had similar effects to S100A16 silencing. Overexpression of S100A16 in GC cells partially reversed the inhibitory effects of the miR-6884-5p mimic. miR-6884-5p inhibited the proliferation, invasion, and EMT of GC cells by directly decreasing S100A16 expression.