MiR-490-3p inhibited the proliferation and metastasis of esophageal squamous cell carcinoma by targeting HMGA2

被引:4
|
作者
Kang, N-N [1 ]
Ge, S-L [2 ]
Zhang, R-Q [1 ]
Huang, Y-L [1 ]
Liu, S-D [2 ]
Wu, K-M [1 ]
机构
[1] Anhui Med Univ, Affiliated Hosp 1, Dept Thorac Surg, Hefei, Anhui, Peoples R China
[2] Anhui Med Univ, Affiliated Hosp 1, Dept Cardiovasc Surg, Hefei, Anhui, Peoples R China
关键词
MiR-490-3p; Esophageal squamous cell carcinoma (ESCC); High-mobility group AT-hook 2 (HMGA2); Epithelial-mesenchymal transition (EMT); EPITHELIAL-MESENCHYMAL TRANSITION; BREAST-CANCER; EXPRESSION; MICRORNA; GROWTH;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
OBJECTIVE: To identify the potential role of miR-490-3p in the development of esophageal squamous cell carcinoma (ESCC), and to explore the possible underlying mechanism. PATIENTS AND METHODS: Human ESCC tissues and cancer-adjacent normal tissues were collected. The mRNA expression level of miR-490-3p was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). On-line target gene prediction software was applied to screen high-mobility group AT-hook 2 (HMGA2). Subsequently, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide), qRT-PCR, Western blotting, transwell and scratch-wound assays were conducted to analyze the effect of miR-490-3p on the biological function of the ESCC cell line (EC-109). RESULTS: In our study, the mRNA expression level of miR-490-3p was remarkably reduced in ESCC tissues and cells. Molecular mechanism analysis confirmed that miR-490-3p could act on the 3'-UTR of HMGA2 and regulate its expression. Subsequent functional experiments indicated that decreased expression of HMGA2 resulting from the up-regulation of miR-490-3p could inhibit the proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) of ESCC cells. CONCLUSIONS: We discovered the inhibitory effect of miR-490-3p on ESCC by targeting HMGA2. and revealed that miR-490-3p could be a potential therapeutic target for ESCC.
引用
收藏
页码:8298 / 8305
页数:8
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