Increased miR-222 in H. pylori-associated gastric cancer correlated with tumor progression by promoting cancer cell proliferation and targeting RECK
- 作者：Na Li ; Bin Tang ; En-Dong Zhu ; Bo-sheng Li ; Yuan Zhuang ; Shu Yu ; Dong-shui Lu ; Quan-Ming Zou ; Bin Xiao ; binxiaotmmu@163.com ; Xu-Hu Mao ; mxh95xy@tom.com
- 关键词：miRNAs ; microRNAs ; H. pylori ; Helicobacter pylori ; RECK ; reversion-inducing cysteine-rich protein with Kazal motifs ; MOI ; multiplicity of infection ; qRT-PCR ; quantitative RT-PCR ; GFP ; green fluorescence protein ; UTR ; untranslated region ; MMPs ; matrix meta
- 刊名：FEBS Letters
- 出版年：2012
- 期刊代码：70_00145793
- 类别：bio
- 出版时间：23 March, 2012
- 卷：586
- 期：6
- 页码：722-728
- 文件大小：1058 K
摘要
Little is known about the potential role of microRNAs (miRNAs) in the carcinogenesis of gastric cancer induced by Helicobacter pylori (H. pylori). Here, we showed that microRNA-222 (miR-222) was up-regulated in H. pylori-infected gastric mucosa and gastric cancer. Ectopic expression of miR-222 promoted cell proliferation and colony formation in vitro. Mechanistically, we identified RECK as a novel target of miR-222, and also confirmed their relationship by the inverse correlation of mRNA expression ex vivo. Furthermore, we found that RNA interference silencing of RECK can mimic the oncogenic effects of miR-222. Collectively, H. pylori may function as an initiator in the process of carcinogenesis by up-regulating miR-222, which further participates in the progression of cancer by promoting proliferation and inhibiting RECK.