Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis

被引:74
作者
Li, Zhongwen [1 ]
Wu, Xiaoliang [2 ,3 ,4 ]
Gu, Ling [3 ,4 ,5 ]
Shen, Qi [2 ]
Luo, Wen [2 ]
Deng, Chuangzhong [3 ,4 ]
Zhou, Qianghua [3 ,4 ]
Chen, Xinru [3 ,4 ]
Li, Yanjie [6 ]
Lim, ZuanFu [7 ]
Wang, Xing [3 ,4 ]
Wang, Jiahong [3 ,4 ,8 ]
Yang, Xianzi [3 ,4 ,8 ]
机构
[1] Zunyi Med Univ, Dept Oncol, Affiliated Hosp, Zunyi, Peoples R China
[2] Guizhou Prov Peoples Hosp, Dept Oncol, Guiyang, Guizhou, Peoples R China
[3] Sun Yat Sen Univ, Canc Ctr, State Key Lab Oncol South China, Guangzhou, Guangdong, Peoples R China
[4] Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, Guangzhou, Guangdong, Peoples R China
[5] Puer Univ, Puer, Peoples R China
[6] Sun Yat Sen Univ, Affiliated Hosp 3, Guangzhou, Guangdong, Peoples R China
[7] West Virginia Univ, Mary Babb Randolph Canc Inst, WVU Canc Inst, Robert C Byrd Hlth Sci Ctr, Morgantown, WV USA
[8] Guangzhou Med Univ, Affiliated Canc Hosp & Inst, 78 Hengzhigang Rd, Guangzhou, Guangdong, Peoples R China
来源
CELL DEATH & DISEASE | 2017年 / 8卷
关键词
INVASION-METASTASIS CASCADE; LNCRNA-ATB; UP-REGULATION; CANCER CELLS; KINDLIN-2; PROGRESSION; INVASIVENESS; PROGNOSIS; EVOLUTION; MIGRATION;
D O I
10.1038/cddis.2017.245
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer-related death, especially in China. In addition, the prognosis of late stage patients is extremely poor. However, the biological significance of the long non-coding RNA lnc-ATB and its potential role in ESCC remain to be documented. In this study, we investigated the role of lnc-ATB and the underlying mechanism promoting its oncogenic activity in ESCC. Expression of lnc-ATB was higher in ESCC tissues and cell lines than that in normal counterparts. Upregulated lnc-ATB served as an independent prognosis predictor of ESCC patients. Moreover, loss-offunction assays in ESCC cells showed that knockdown of lnc-ATB inhibited cell proliferation and migration both in vitro and in vivo. Mechanistic investigation indicated that lnc-ATB exerted oncogenic activities via regulating Kindlin-2, as the anti-migration role of lnc-ATB silence was attenuated by ectopic expression of Kindlin-2. Further analysis showed that lnc-ATB functions as a molecular sponge for miR-200b and Kindlin-2. Dysregulated miR-200b/Kindlin-2 signaling mediated the oncogenic activity of lnc-ATB in ESCC. Our results suggest that lnc-ATB predicts poor prognosis and may serve as a potential therapeutic target for ESCC patients.
引用
收藏
页码:e2888 / e2888
页数:11
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