Long noncoding RNA FBXL19-AS1 induces tumor growth and metastasis by sponging miR-203a-3p in lung adenocarcinoma

被引:25
|
作者
Wang, Liming [1 ]
Zhang, Xin [1 ]
Liu, Yang [2 ]
Xu, Shun [1 ]
机构
[1] China Med Univ, Affiliated Hosp 1, Dept Thorac Surg, 155 North Nanjing St, Shenyang 110001, Liaoning, Peoples R China
[2] China Med Univ, Affiliated Hosp 1, Dept Pharm, Shenyang, Liaoning, Peoples R China
关键词
FBXL19-AS1; LncRNA; lung adenocarcinoma; miR-203a-3p; EPITHELIAL-MESENCHYMAL TRANSITION; CELL-PROLIFERATION; DOWN-REGULATION; MESSENGER-RNAS; CANCER CELLS; APOPTOSIS; MIGRATION; INVASION; ACTIVATION; EXPRESSION;
D O I
10.1002/jcp.29251
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The pivotal roles of long noncoding RNAs have been reported in various cancers. Recently, FBXL19-AS1 was proposed to be involved in tumor progression. However, its role in lung adenocarcinoma (LUAD) remains elusive. In this study, we observed that FBXL19-AS1 was significantly upregulated in LUAD tissues and high FBXL19-AS1 expression in LUAD was associated with a poor prognosis. Nevertheless, miR-203-3p showed the opposite effect. Moreover, cell viability and apoptosis analysis revealed that FBXL19-AS1 knockdown could arrest LUAD cells in G0/G1 phase and inhibit cell proliferation, migration and invasion in vitro and inhibited LUAD tumor progress in vivo. Mechanistically, we identified FBXL19-AS1 could act as a miR-203a-3p sponge using dual-luciferase reporter assay. In addition, we demonstrated that downregulation of miR-203a-3p reversed growth inhibition of LUAD cells caused by FBXL19-AS1 knockdown. Finally, FBXL19-AS1/miR-203a-3p axis was found to associate with baculoviral IAP repeat-containing protein 5.1-A-like (survivin), distal-less homeobox 5, E2F transcription factor 1, and zinc finger E-box binding homeobox 2 to regulate metastasis in LUAD cells. This study reveals a significance and mechanism of FBXL19-AS1 in LUAD proliferation and metastasis and offers a potential prognostic marker and a therapeutic target for patients with LUAD.
引用
收藏
页码:3612 / 3625
页数:14
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