Long non-coding RNA MINCR promotes gallbladder cancer progression through stimulating EZH2 expression

被引:59
作者
Wang, Shou-Hua [1 ]
Yang, Yong [1 ]
Wu, Xiao-Cai [1 ]
Zhang, Ming-Di [1 ]
Weng, Ming-Zhe [1 ]
Zhou, Di [1 ]
Wang, Jian-Dong [1 ]
Quan, Zhi-Wei [1 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Dept Gen Surg, Xinhua Hosp, Shanghai 200000, Peoples R China
基金
中国国家自然科学基金;
关键词
MYC-induced long non-coding RNA; miR-26a-5p; Enhancer of zeste homolog 2; Competing endogenous RNA; Gallbladder cancer; HUMAN HEPATOCELLULAR-CARCINOMA; LIVER-CANCER; NASOPHARYNGEAL CARCINOMA; DNA METHYLATION; PROSTATE-CANCER; C-MYC; MIR-26A; MICRORNA-26A; REPRESSION; TUMORIGENESIS;
D O I
10.1016/j.canlet.2016.06.019
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The regulation of MYC-regulated long non-coding RNAs has been reported to contribute to certain types of cancers. However, the role of MYC-induced long non-coding RNA (MINCR) in the tumorigenesis of gallbladder cancer (GBC) is still largely unknown. In this study, we discovered that MINCR was markedly upregulated in GBC tissues compared with adjacent normal tissues. High MINCR expression levels in GBC were positively associated with tumor volume and lymph node metastasis and were negatively correlated with overall survival (OS). Upregulation of MINCR and enhancer of zeste homolog 2 (EZH2) in GBC coincided with the downregulation of miR-26a-5p in GBC. Mechanistically, MINCR/miR-26a-5p/EZH2 axis was found to be involved in cell proliferation, cell invasive and apoptosis in GBC cells. Moreover, knockdown of MINCR suppressed cell proliferation, decreased S-phase cell numbers, increased cell apoptosis, and inhibited cell invasion by inhibiting the epithelial-mesenchymal transition (EMT) phenomenon in GBC cells. In vivo, tumor volumes were significantly decreased in the MINCR silencing group compared with those in the control group. These results demonstrated that MINCR could potentially be a therapeutic target as well as a prognostic marker in GBC. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:122 / 133
页数:12
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