Long Non-coding RNA Colon Cancer-Associated Transcript-1 Promotes Migration, Invasion, and Epithelial Mesenchymal Transition of Lung Adenocarcinoma by Suppressing miR-219-1

被引:4
|
作者
Wang, Wenbo [1 ]
Hou, Zhiliang [1 ]
Wen, Chengcai [2 ,3 ]
Ge, Liyue [3 ,4 ]
Ge, Lili [3 ,5 ]
机构
[1] Henan Prov Chest Hosp, Dept Thorac Surg, Zhengzhou, Peoples R China
[2] Xuzhou Med Univ, Huaian Peoples Hosp 2, Huaian, Peoples R China
[3] Xuzhou Med Univ, Affiliated Huaian Hosp, Huaian, Peoples R China
[4] Xuzhou Med Univ, Huaian Peoples Hosp 2, Dept Oncol, Huaian, Peoples R China
[5] Xuzhou Med Univ, Huaian Peoples Hosp 2, Dept Clin Lab, Huaian, Peoples R China
关键词
lung adenocarcinoma; colon cancer-associated transcript-1; miR-219-1; epithelial-mesenchymal transition; invasion; CCAT1;
D O I
10.3389/fgene.2020.00929
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Previous evidence suggests that long non-coding colon cancer-associated transcript-1(CCAT1) plays a pivotal role in the progression of a variety of tumors. However, little is known about its role in lung adenocarcinoma (LAD). In this study, we found LAD tissue samples had a higher expression of CCAT1 but a lower expression of miR-219-1 compared to their adjacent non-tumor tissues. CCAT1 negatively regulated the expression of miR-219-1. miR-219-1 suppressed the proliferation of A549 and H1299 cells. Knockdown of CCAT1 inhibited the proliferation, migration, and invasion of A549 and H1299 cells, which were reversed by the miR-219-1 inhibitor. CCAT1 knockdown increased the expression of E-cadherin but decreased the expressions of N-cadherin and vimentin, which were restored by the miR-219-1 inhibitor. In vivo, knockdown of CCAT1 suppressed the tumor growth of LAD xenografts, which were rescued by the inhibition of miR-219-1. In summary, our findings suggested that CCAT1 promotes the progression of LAD via sponging miR-219-1, providing a potential therapeutic target for LAD.
引用
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页数:10
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