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- W1418740046 abstract "Background: Dysregulated expression of microRNAs is often found in gastric cancer, and it contributes to the pathogenesis of gastric cancer via regulation of the cell cycle, proliferation, apoptosis, migration, and invasion. Aim: In this study, we aimed to investigate the role of miR-367 in the invasion and metastasis of gastric cancer. Methods: The correlation between the expression level of miR-367 and the clinicopathologic features of 37 patients with gastric cancer was analyzed by using real-time polymerase chain reaction (RT-PCR). In addition, we investigated the effect of miR-367 on the invasion and migration of the gastric cancer cell lines HS746T and SGC-7901 using transwell and scratch-wound assays, and the target gene of miR-367 was predicated and demonstrated by the bioinformatics method and luciferase reporter system, respectively. Results: The results showed that the expression of miR-367 was significantly reduced in the gastric cancer tissues compared with the paraneoplastic tissues, and significantly correlated with the differentiation level, tumor-node-metastasis (TNM) stage, and metastasis of gastric cancer. Notably, the overexpression of miR-367 in gastric cancer cells inhibited the cellular migration and invasion. Furthermore, the luciferase reporter system demonstrated that Rab23 was a target gene of miR-367, and ectopic expression of Rab23 could reverse the invasion and migration inhibitory activity of miR-367. Conclusions: Our study shows that miR-367 is a key negative regulator of the invasion and metastasis of gastric cancer and establishes a strong rationale for developing miR-367 as a novel therapeutic agent against gastric cancer." @default.
- W1418740046 created "2016-06-24" @default.
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- W1418740046 date "2015-02-01" @default.
- W1418740046 modified "2023-10-18" @default.
- W1418740046 title "The microRNA-367 Inhibits the Invasion and Metastasis of Gastric Cancer by Directly Repressing Rab23" @default.
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- W1418740046 doi "https://doi.org/10.1089/gtmb.2014.0210" @default.
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