微小RNA-218通过调控Bmi-1/Akt信号通路抑制胃癌发生。
miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway.
作者信息
Wu Yongxing, Tian Sijia, Chen Yijun, Ji Meiju, Qu Yiping, Hou Peng
机构信息
Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, PR China.
Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, PR China.
出版信息
Pathol Res Pract. 2019 Feb;215(2):243-250. doi: 10.1016/j.prp.2018.10.031. Epub 2018 Oct 28.
BACKGROUND
Previous studies indicated that miR-218 was deregulated in gastric cancer patients and correlated with tumor invasion and prognosis. The aim of this study was to clarify the effect of miR-218 on the malignant behavior of gastric cancer and its role in regulating Bmi-1/Akt signaling pathway.
MATERIALS AND METHODS
We used miR-218 mimic to transfect gastric cancer cell lines AGS and SGC-7901, and the overexpression efficiency was validated using qRT-PCR assay. MTT assay and Transwell chamber system were performed to detect the effect of miR-218 on cell proliferation, invasion and migration on gastric cancer. Western blot and qRT-PCR assay was used to test the role of miR-218 in regulating Bmi-1/Akt signaling pathway.
RESULTS
As shown in our research, ectopic expression of miR-218 in gastric cancer cells inhibits the proliferation, invasion and migration of gastric cancer cells. In addition, miR-218 re-expression inhibits the expression of Bmi-1 and its downstream target p-Akt, as well as MMPs and EMT process.
CONCLUSIONS
miR-218 inhibits the proliferation, invasion and migration of gastric cancer cells through modulating EMT process and the expression of MMPs via Bmi-1/Akt signaling pathway.
背景
先前的研究表明，miR-218在胃癌患者中表达失调，且与肿瘤侵袭和预后相关。本研究旨在阐明miR-218对胃癌恶性行为的影响及其在调节Bmi-1/Akt信号通路中的作用。
材料与方法
我们使用miR-218模拟物转染胃癌细胞系AGS和SGC-7901，并通过qRT-PCR检测验证过表达效率。采用MTT法和Transwell小室系统检测miR-218对胃癌细胞增殖、侵袭和迁移的影响。利用蛋白质免疫印迹法和qRT-PCR检测miR-218在调节Bmi-1/Akt信号通路中的作用。
结果
如我们的研究所显示，miR-218在胃癌细胞中的异位表达抑制了胃癌细胞的增殖、侵袭和迁移。此外，miR-218的重新表达抑制了Bmi-1及其下游靶点p-Akt的表达，以及基质金属蛋白酶（MMPs）的表达和上皮-间质转化（EMT）过程。
结论
miR-218通过Bmi-1/Akt信号通路调节EMT过程和MMPs的表达，从而抑制胃癌细胞的增殖、侵袭和迁移。
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