miR-30a-5p functions as a tumor suppressor gene in gastric cancer

Identification: 2064


Description

miR-30a-5p functions as a tumor suppressor gene in gastric cancer

Jimin Min1, Tae-Su Han1, 3, Boram Choi1, Keun Hur4, Kazuyoshi Yanagihara5,

V Narry Kim6, Hyuk-Joon Lee1, 2 and Han-Kwang Yang1, 2

1Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea;

2Department of Surgery, Seoul National University College of Medicine, Seoul, Korea;

3Division of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan;

4Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Daegu, Korea;

5National Cancer Center Research Institute, Tokyo, Japan;

6School of Biological Sciences, Seoul National University, Seoul, Korea

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. Taken together, the miR-30a-5p expression was frequently down-regulated in GC. 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.

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