Article ID Journal Published Year Pages File Type
2048489 FEBS Letters 2012 7 Pages PDF
Abstract

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.

► miR-222 is up-regulated both by H. pylori infection and in gastric cancer. ► Over-expression of miR-222 promotes cell proliferation and colony formation. ► RECK is a novel target of miR-222 and inversely correlated with miR-222. ► RECK is involved in miR-222-regulated proliferation in gastric cancer cells.

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