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首页> 外文期刊>FEBS letters. >Increased miR-222 in H. pylori-associated gastric cancer correlated with tumor progression by promoting cancer cell proliferation and targeting RECK
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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

机译:通过促进癌细胞增殖和靶向RECK,幽门螺杆菌相关性胃癌中miR-222的增加与肿瘤进展相关

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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.
机译:关于microRNA(miRNA)在幽门螺杆菌(H. pylori)诱导的胃癌致癌作用中的潜在作用知之甚少。在这里,我们显示microRNA-222(miR-222)在幽门螺杆菌感染的胃黏膜和胃癌中被上调。 miR-222的异位表达促进体外细胞增殖和集落形成。从机理上讲,我们将RECK鉴定为miR-222的新靶标,并通过离体mRNA表达的负相关来证实它们之间的关系。此外,我们发现RECK的RNA干扰沉默可以模仿miR-222的致癌作用。幽门螺杆菌可通过上调miR-222在致癌过程中起引发剂的作用,miR-222通过促进增殖和抑制RECK进一步参与癌症的发展。

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