miR-1294 通过抑制胃癌中的 FOXK1 缓解上皮-间充质转化。
miR-1294 alleviates epithelial-mesenchymal transition by repressing FOXK1 in gastric cancer.
机构信息
Department of Gastroenterology, The First Affiliated Hospital of Shandong First Medical University, Jinan, 250014, Shandong, China.
Department of Gastroenterology, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, 130021, Jilin, China.
出版信息
Genes Genomics. 2020 Feb;42(2):217-224. doi: 10.1007/s13258-019-00899-3. Epub 2019 Dec 12.
BACKGROUND
MicroRNAs (miRNAs) have been reported play critical roles in regulating tumor development and progression.
OBJECTIVE
This study aimed to investigate the potential effect of miR-1294 in gastric cancer (GC).
METHODS
Reverse transcription quantitative polymerase chain reaction (RT-PCR) were performed to verify the expression level of miR-1294 and Forkhead box protein K1 (FOXK1). Overall survival data of miR-1294 for GC was analysed by log-rank test. Targetscan was used to screen potential target gene of miR-1294. Dual luciferase assay was assessed to investigate the relationship between miR-1294 and FOXK1. The miR-1294 overexpression and knockdown were designed to study the biological function of miR-1294. The migration and invasion of GC cell lines were investigated by wound healing and transwell assays. Western blotting were performed to verify the expression level of epithelial marker, mesenchymal markers and FOXK1. Overexpression of FOXK1 was designed to study the rescue effects of FOXK1 in SGC7901 cell.
RESULTS
miR-1294 was found downregulated in GC patients and cell lines. A higher miR-1294 expression showed a significant longer overall survival than those with a lower miR-1294 expression. miR-1294 directly targets FOXK1 and regulates the expression of FOXK1. In addition, miR-1294 regulates epithelial-mesenchymal transition (EMT) by inhibiting FOXK1 in GC cells and it can be rescued by overexpression of FOXK1.
CONCLUSION
miR-1294 alleviates EMT process in GC by targeting FOXK1.
背景
MicroRNAs（miRNAs）已被报道在调控肿瘤发生和发展中发挥关键作用。
目的
本研究旨在探讨 miR-1294 在胃癌（GC）中的潜在作用。
方法
采用逆转录定量聚合酶链反应（RT-PCR）验证 miR-1294 和 Forkhead box 蛋白 K1（FOXK1）的表达水平。采用对数秩检验分析 miR-1294 对 GC 患者总生存期的影响。Targetscan 用于筛选 miR-1294 的潜在靶基因。双荧光素酶报告基因实验验证 miR-1294 与 FOXK1 的关系。设计 miR-1294 过表达和敲低实验研究 miR-1294 的生物学功能。通过划痕愈合和 Transwell 实验研究 GC 细胞系的迁移和侵袭能力。Western blot 检测上皮标志物、间充质标志物和 FOXK1 的表达水平。设计过表达 FOXK1 实验研究 FOXK1 在 SGC7901 细胞中的拯救作用。
结果
miR-1294 在 GC 患者和细胞系中表达下调。miR-1294 高表达的患者总生存期显著长于 miR-1294 低表达的患者。miR-1294 直接靶向 FOXK1 并调节 FOXK1 的表达。此外，miR-1294 通过抑制 FOXK1 在 GC 细胞中调节上皮-间充质转化（EMT），并可通过过表达 FOXK1 得到拯救。
结论
miR-1294 通过靶向 FOXK1 减轻 GC 中的 EMT 过程。
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