miR-1236-3p inhibits invasion and metastasis in gastric cancer by targeting MTA2

被引:56
作者
An, Jia-Xiang [1 ]
Ma, Ming-Hui [1 ]
Zhang, Chun-Dong [1 ]
Shao, Shuai [1 ]
Zhou, Nuo-Ming [1 ]
Dai, Dong-Qiu [1 ]
机构
[1] China Med Univ, Affiliated Hosp 4, Dept Gastroenterol Surg, Shenyang 110032, Liaoning, Peoples R China
关键词
Gastric cancer; Metastasis; miR-1236-3p; MTA2; Epithelial-mesenchymal transition; Tumor suppressor gene; PROMOTES; PROLIFERATION; SURVIVAL; OVEREXPRESSION; PROGRESSION; PREDICTION; PROTEIN-2; MIRNAS; GROWTH; ALPHA;
D O I
10.1186/s12935-018-0560-9
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Background: MicroRNAs deregulation are common in human tumor progression. miR-1236-3p has been reported to function as tumor suppressor microRNA in various malignancies. The aim of this study was to demonstrate the downregulated expression of miR-1236-3p in gastric cancer (GC) tissues and cell lines, and clarify its biological function in GC. Methods: Real-time polymerase chain reaction was used to measure the mRNA level of miR-1236-3p in GC. Dual luciferase assay was used to demonstrate that MTA2 was one of the candidate target genes of miR-1236-3p. Western blots were utilized to detect the protein levels. Cell function assays were also performed to determine the function of miR-1236-3p in GC. Results: miR-1236-3p expression, which was associated with lymph node metastasis, differentiation and clinical stage, was significantly reduced in GC tissues and cell lines. miR-1236-3p over-expression could inhibit GC cell proliferation, migration and invasion, and inhibition of miR-1236-3p expression had opposite effects. Furthermore, we demonstrated that MTA2 was a candidate target of miR-1236-3p, and miR-1236-3p over-expression significantly inhibited the process of epithelial-mesenchymal transition. We also found that miR-1236-3p could suppress the PI3K/Akt signaling pathway in GC cells. Conclusions: Our results suggest that miR-1236-3p functions as a tumor suppressor in GC and could be a promising therapeutic target for GC.
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页数:11
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