Abstract
Abstract Objectives: To expore miRNA expression pattern in gastric cancer and investigate the role of miRNAs in the tumorigenesis of gastric cancer. Methods: We globally analyzed the miRNA expression profile in 9 gastric cancer cell lines and 6 normal gastric mucosa and the tumor tissues and its corespending adjacent normal tisuues of 30 patients through miRNA microarray. The differential expression of miRNAs from miRNA microarray were confirmed by qRT-PCR. Then, we extended our assay to sixty paired gastric cancer tissues and the relationship between miR-126 expression level and clinicopatholoic variables was explored. The specific miR-126 precursor or miR-126 expression vector were transfected into gastric cancer cell line SGC-7901 to up-regulate miR-126 expression and its biological effects on SGC-7901 cells were investigated. Finally, the target gene of miR-126 was predicted by bioimformatic method and validated by luciferase reportor system. Results: found that 17 miRNAs were up-regulated in gastric cancer cell lines and 146 miRNAs were down-regulated compared with normal gastric mucosa. Then we performed quantitative real-time PCR of 15 up-regulated miRNAs and 26 logRatio < –5.0 down-regulated miRNAs in gastric cancer cell lines and gastric cancer tissues for further analysis. The coincidence of microarray data and qPCR results was in an acceptable range and 15 miRNAs were finally selected. These candidate miRNAs were associated with gastric cancer clinicopathology in different degree. Meanwhile, high expression of hsa-miR-93 and hsa-miR-409-3p were found to predict poor survival (median, 16 months vs 40 months, LogRank p < 0.05). we show that miR-126 is significantly down-regulated in gastric cancer tissues and associated with clinicopathological features such as tumor size, lymph node metastasis, local invasion and TNM stage. Ectopic expression of miR-126 in SGC-7901 gastic cancer cells potently inhibits cell growth by inducing cell cycle arrest at G1 phase, migration and invasion in vitro and tumorigenicity in vivo. Mechanistically, we identify adaptor protein Crk as a target of miR-126. Taken together, our findings demonstrate miR-126 may function as a tumor suppressor in gastric cancer through regulation of genes such as Crk. Conclusions: These findings may suggest vital roles of miRNAs in huamn gastric cancer, and provide clues for understanding the molecular basis of miRNAs in various biological processes. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4141. doi:1538-7445.AM2012-4141
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