Down-regulation of lncRNA CASC2 promotes cell proliferation and metastasis of bladder cancer by activation of the Wnt/β-catenin signaling pathway

被引:91
作者
Pei, Zhijun [1 ,2 ]
Du, Xian [3 ]
Song, Yafeng [1 ,2 ]
Fan, Lin [4 ]
Li, Fuyan [1 ,2 ]
Gao, Yan [1 ,2 ]
Wu, Ruimin [1 ,2 ]
Chen, Yijia [1 ,2 ]
Li, Wei [1 ,2 ]
Zhou, Hong [1 ,2 ]
Yang, Yi [1 ,2 ]
Zeng, Jing [5 ]
机构
[1] Hubei Univ Med, Taihe Hosp, Dept PET Ctr, Shiyan, Hubei Province, Peoples R China
[2] Hubei Univ Med, Taihe Hosp, Inst Anesthesiol & Pain, Shiyan, Hubei Province, Peoples R China
[3] Hubei Univ Med, Taihe Hosp, Dept Gen Surg 2, Shiyan 442000, Hubei Province, Peoples R China
[4] Hubei Univ Med, Taihe Hosp, Dept Ophthalmol, Shiyan 442000, Hubei Province, Peoples R China
[5] Hubei Univ Med, Taihe Hosp, Dept Infect Control, Shiyan 442000, Hubei Province, Peoples R China
基金
中国国家自然科学基金;
关键词
bladder cancer; CASC2; Wnt/beta-catenin; proliferation; metastasis; POOR-PROGNOSIS; RNA; SUPPRESSES; EXPRESSION; MIGRATION; INCREASES; INVASION;
D O I
10.18632/oncotarget.15210
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Long noncoding RNAs cancer susceptibility candidate 2 (CASC2) have been demonstrated as playing crucial regulatory roles in a few of cancers. However, the biological function of lncRNA CASC2 in bladder cancer are still unclear. In this study, we found that lncRNA CASC2 was significantly down-regulated in bladder cancer tissues and cell lines by quantitative real time-PCR and associated with advanced TNM stage (III/IV). Moreover, overexpression of lncRNA CASC2 remarkably reduced the cell growth, migration and invasion, as well as promoted early apoptosis of bladder cancer cell in vitro. Furthermore, we illustrated that lncRNA CASC2 inhibited Wnt/beta-catenin signal pathway activity by decrasing the beta-catenin expression and reversing the downstream target gene expression of Wnt signaling pathway. Taken together, lncRNA CASC2 plays an pivotal role in bladder tumorigenesis and progression and may act as a potential biomarker for the treatment of bladder cancer.
引用
收藏
页码:18145 / 18153
页数:9
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