长链非编码RNA linc-UBC1通过调控EZH2和抑制食管鳞状细胞癌中的E-钙黏蛋白来促进肿瘤侵袭和转移。
Long noncoding RNA linc-UBC1 promotes tumor invasion and metastasis by regulating EZH2 and repressing E-cadherin in esophageal squamous cell carcinoma.
作者信息
Niu Guangcai, Zhuang Huijie, Li Bingqiang, Cao Gang
机构信息
Department of Oncological Surgery, Xuzhou Central Hospital, Xuzhou, China.
出版信息
J BUON. 2018 Jan-Feb;23(1):157-162.
PURPOSE
Recent reports have shown that long noncoding (lnc) RNAs are critical during tumorigenesis. This study focused on the influence of linc-UBC1 on the metastasis of esophageal squamous cell carcinoma (ESCC) and the underlying mechanism.
METHODS
In 50 ESCC tissues and 5 ESCC cell lines, linc- UBC1 expression was detected by RT-qPCR. Moreover, correlation analysis was conducted between linc-UBC1 expression level and clinicopathological features. Overall survival of these ESCC patients was analyzed by Kaplan-Meier method. In addition, wound healing assay and cell invasion assay were utilized to identify whether linc-UBC1 could affect the migration and invasion ability of ESCC cells. Western blotting and luciferase assay were used to explore the potential mechanism.
RESULTS
In ESCC tissues, linc-UBC1 expression level was significantly higher and was remarkably related with clinical features such as TNM stage and nodal metastasis. Meanwhile, overall survival of ESCC patients with high expression of linc-UBC1 was significantly worse than that of patients with low expression. Besides, the migration and invasion ability of ESCC cells was inhibited via knockdown of linc-UBC1. Further study showed that knockdown of linc-UBC1 could suppress the protein level of EZH2 and promote the protein level of E-cadherin.
CONCLUSIONS
The results indicate that linc-UBC1 is a novel oncogene in tumorigenesis and could promote the metastasis via EZH2 and E-cadherin, which may offer a possible therapeutic target in ESCC.
目的
近期报告显示长链非编码(lnc)RNA在肿瘤发生过程中至关重要。本研究聚焦于linc-UBC1对食管鳞状细胞癌(ESCC)转移的影响及其潜在机制。
方法
采用RT-qPCR检测50例ESCC组织和5种ESCC细胞系中linc-UBC1的表达。此外,对linc-UBC1表达水平与临床病理特征进行相关性分析。采用Kaplan-Meier法分析这些ESCC患者的总生存期。另外,利用伤口愈合试验和细胞侵袭试验来确定linc-UBC1是否会影响ESCC细胞的迁移和侵袭能力。采用蛋白质印迹法和荧光素酶试验探索潜在机制。
结果
在ESCC组织中,linc-UBC1表达水平显著更高,且与TNM分期和淋巴结转移等临床特征显著相关。同时,linc-UBC1高表达的ESCC患者的总生存期明显差于低表达患者。此外,敲低linc-UBC1可抑制ESCC细胞的迁移和侵袭能力。进一步研究表明,敲低linc-UBC1可抑制EZH2蛋白水平并促进E-钙黏蛋白的蛋白水平。
结论
结果表明linc-UBC1是肿瘤发生过程中的一种新型癌基因,可通过EZH2和E-钙黏蛋白促进转移,这可能为ESCC提供一个潜在的治疗靶点。