THUMPD3-ASI Is Correlated With Non-Small Cell Lung Cancer And Regulates Self-Renewal Through miR-543 And ONECUT2

被引：34
作者：
Hu, Jia [1 ]
Chen, Youfang [1 ]
Li, Xiaodong [1 ]
Miao, Huikai [1 ]
Li, Rongzhen [1 ]
Chen, Dongni [1 ]
Wen, Zhesheng [1 ]
机构：
[1] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, Dept Thorac Oncol, State Key Lab Oncol South China,Canc Ctr, Guangzhou 510060, Peoples R China
来源：
ONCOTARGETS AND THERAPY | 2019年 / 12卷
基金：
中国国家自然科学基金;
关键词：
non-small cell lung cancer; self-renewal; THUMPD3-AS1; miR-543; ONECUT2; LONG NONCODING RNAS; MICRORNAS; CERNA; ERA;
D O I：
10.2147/OTT.S227995
中图分类号：
Q81 [生物工程学（生物技术）]; Q93 [微生物学];
学科分类号：
071005 ; 0836 ; 090102 ; 100705 ;
摘要：
Background: Of all malignancies, lung cancer is the leading cause of death, and non-small cell lung cancer (NSCLC) accounts for 80-85% of all lung cancers. In this study, the long non-coding RNA (lncRNA) THUMPD3-AS1 was observed to be highly expressed in NSCLC and correlated with TNM stages and relapse, suggesting that THUMPD3-AS1 is involved in the regulation of NSCLC. Methods: The aim of this study was to investigate the regulatory function and mechanism of THUMPD3-AS1 in NSCLC cells by cellular function and molecular biology experiments. Results: Overexpression and knockdown analysis revealed that THUMPD3-AS1 promoted tumor progression by increasing cell proliferation and self-renewal of NSCLC cells. Moreover, THUMPD3-AS1 may act as an endogenous sponge of microRNA-543 (miR-543) which can regulate the target gene ONECUT2 in NSCLC cells. Conclusion: Our study indicated that THUMPD3-AS1 regulated NSCLC cell self-renewal by regulating the expression of miR-543 and ONECUT2, and THUMPD3-AS1 can potentially act as a biomarker or therapeutic target in NSCLC.
引用
收藏
页码：9849 / 9860
页数：12
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