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

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 rela...

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Published inOncoTargets and therapy p. 9849
Main Authors Hu, Jia, Chen, Youfang, Li, Xiaodong, Miao, Huikai, Li, Rongzhen, Chen, Dongni, Wen, Zhesheng
Format Journal Article
LanguageEnglish
Published Dove Medical Press Limited 01.11.2019
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Abstract 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 (miR543) 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. Keywords: non-small cell lung cancer, self-renewal, THUMPD3-AS1, miR-543, ONECUT2
AbstractList 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 (miR543) 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. Keywords: non-small cell lung cancer, self-renewal, THUMPD3-AS1, miR-543, ONECUT2
Audience Academic
Author Hu, Jia
Miao, Huikai
Wen, Zhesheng
Li, Xiaodong
Li, Rongzhen
Chen, Youfang
Chen, Dongni
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Snippet 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...
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SubjectTerms Analysis
Death
Genes
Health aspects
Lung cancer
MicroRNA
Molecular biology
Non-small cell lung cancer
RNA
Small cell lung cancer
Tumors
Title THUMPD3-ASI Is Correlated With Non-Small Cell Lung Cancer And Regulates Self-Renewal Through miR-543 And ONECUT2
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