分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

miRNA‑30a‑3p inhibits metastasis and enhances radiosensitivity in esophageal carcinoma by targeting insulin‑like growth factor 1 receptor

Yanxin Fan, Xiuhua Bian, Pudong Qian, Jing Wen, Pengwei Yan, Yanhong Luo, Jing Wu, Qian Zhang

Journal:Molecular Medicine Reports

IF:1.85

DOI:10.3892/mmr.2019.10222

PMID:31115568

Published:2019-05-09

research field:肿瘤学分子生物学癌症生物学

Abstract

It has been demonstrated that microRNAs (miRNAs) serve important roles in various biological processes, such as tumorigenesis. In the present study, the role of miR‑30a‑3p in the pathogenesis of esophageal carcinoma (EC) was investigated. Reverse transcription‑quantitative polymerase chain reaction was performed to determine the levels of miR‑30a‑3p expression in EC tissues and cell lines. Then, the effects of miR‑30a‑3p on the migration, invasion and radiosensitivity of EC cells were investigated using scratch‑wound, Transwell and radiosensitivity assays, respectively. A dual‑luciferase reporter assay was performed to determine potential interactions between miR‑30a‑3p and the 3'‑untranslated region (3'‑UTR) of insulin‑like growth factor 1 receptor (IGF‑1R). The results demonstrated that the levels of miR‑30a‑3p expression in EC tissues and cell lines were significantly decreased compared with those in paired healthy tissues and a human esophageal epithelial cell line. Upregulation of miR‑30a‑3p expression significantly suppressed migration, invasion and epithelial‑mesenchymal transition (EMT), and enhanced radiosensitivity in EC cells. Analysis of luciferase activity demonstrated that miR‑30a‑3p interacted with the 3'‑UTR of IGF‑1R, and knockdown of IGF‑1R induced similar effects on the migration, invasion, EMT and radiosensitivity of EC cells. The results indicated that miR‑30a‑3p suppressed metastasis and enhanced the radiosensitivity of EC cells via downregulation IGF‑1R, suggesting that miR‑30a‑3p may be a potential therapeutic target in the treatment of EC.

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