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Increased miR‐222 in H. pylori ‐associated gastric cancer correlated with tumor progression by promoting cancer cell proliferation and targeting RECK
Author(s) -
Li Na,
Tang Bin,
Zhu En-Dong,
Li Bo-sheng,
Zhuang Yuan,
Yu Shu,
Lu Dong-shui,
Zou Quan-Ming,
Xiao Bin,
Mao Xu-Hu
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.01.025
Subject(s) - ectopic expression , microrna , helicobacter pylori , cancer , gene silencing , carcinogenesis , cancer research , cell growth , rna interference , biology , tumor progression , rna , cell culture , gene , biochemistry , genetics
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.