MicroRNA-146b-5p inhibits the growth of gallbladder carcinoma by targeting epidermal growth factor receptor

被引:48
作者
Cai, Jingli [1 ,2 ]
Xu, Lubai [2 ]
Cai, Zhenzhai [3 ]
Wang, Jisheng [2 ]
Zhou, Bing [2 ]
Hu, Hai [1 ]
机构
[1] Tongji Univ, Sch Med, Dept Gen Surg, East Hosp, Shanghai 200120, Peoples R China
[2] Wenzhou Med Univ, Affiliated Hosp 2, Dept Gen Surg, Wenzhou 325000, Zhejiang, Peoples R China
[3] Wenzhou Med Univ, Affiliated Hosp 2, Dept Gastroenterol, Wenzhou 325000, Zhejiang, Peoples R China
关键词
microRNA-146b-5p; gallbladder cancer; epidermal growth factor receptor; CANCER CELLS; EXPRESSION; MIR-146B-5P; METASTASIS; MANAGEMENT; MIGRATION; INVASION; THERAPY; EGFR;
D O I
10.3892/mmr.2015.3461
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Gallbladder cancer (GBC) is the most common and aggressive type of biliary tract cancer. The study of potential treatments for GBC has recently focused on microRNAs, a class of small non-coding RNAs, which post-transcriptionally regulate gene expression during various crucial cell processes. The present study aimed to investigate the role of microRNA-146b (miR-146b) in GBC. Human GBC tissue and adjacent normal gallbladder tissue sections were surgically removed and miR-146b-5p expression and the development and pathological characteristics of GBC were investigated. miR-146b-5p expression was reduced in GBC tissue compared with that in adjacent tissue, and a significant correlation was observed between miR-146b-5p expression levels and carcinoma size and development. miR-146b-5p overexpression in the SGC-996 GBC cell line inhibited cell growth through enhanced apoptosis and G(1) phase arrest. Furthermore, it was demonstrated that epidermal growth factor receptor (EGFR) was regulated directly by miR-146b-5p and was essential as a mediator of the biological effects of miR-146b-5p in GBC. Enforced expression of EGFR reversed the ability of miR-146b-5p to inhibit proliferation. In conclusion, the present study indicated that the mechanism of action of miR-146b-5p in GBC involves the regulation of EGFR expression.
引用
收藏
页码:1549 / 1555
页数:7
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