Abstract

Abstract Gastric cancer (GC) is the second leading cause of cancer-related death. MicroRNAs(miRNAs) are an abundant class of negative gene regulator and regulate multiple gene targets. miRNAs control a wide range of biological functions such as cellular proliferation, differentiation and apoptosis. Moreover, many miRNAs are highly conserved, and their deregulation is often associated with human malignancies. The aims of this study are to determine the miR-30a functions as a tumor suppressor gene and to evaluate whether the miR-30a-5p is able to use the diagnostic or prognostic marker in GC. To identify the gastric tumor-associated miRNAs, miRNA microarray was performed using the gastric cancer tissues. Among them, miR-30a-5p was down-regulated in GC tissues compared to normal mucosa. qRT-PCR was employed to confirm the microarray results. MiR-30a-5p expression was frequently down-regulated in our GC cohort, (n = 55, P<0.0001). To determine the miR-30a-5p biological functions in GC, miR-30a-5p mimic or inhibitor was treated in GC cell lines. Ectopic expression of miR-30a-5p decreased cell growth, migration capacity and colony formation in vitro. Some previous studies have elucidated that miR-30a-5p is associated with metastasis in some cancer types. Accordingly, we confirmed its expression in our GC cohort with lymph node metastasis (n = 13) using qRT-PCR. MiR-30a-5p was significantly down-regulated in lymph node metastasis tissues than normal or tumor tissues. Taken together, the miR-30a-5p expression was frequently down-regulated in GC and lymph node metastasis. In addition, the miR-30a-5p suppressed tumorigenesis. Therefore, we suggest that miR-30a-5p activation may be a useful strategy of GC patient therapy and it can serve as a diagnostic or prognostic marker for GC. Citation Format: Jimin Min, Tae-su Han, Boram Choi, Keun Hur, Hyuk-Joon Lee, Han-Kwang Yang. miR-30a-5p functions as a tumor suppressor gene in gastric cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3115. doi:10.1158/1538-7445.AM2015-3115

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