THUMPD3-AS1 Is Correlated With Non-Small Cell Lung Cancer And Regulates Self-Renewal Through miR-543 And ONECUT2

Jia Hu; Youfang Chen; Xiaodong Li; Huikai Miao; Rongzhen Li; Dongni Chen; Zhesheng Wen

doi:10.2147/OTT.S227995

THUMPD3-AS1 Is Correlated With Non-Small Cell Lung Cancer And Regulates Self-Renewal Through miR-543 And ONECUT2

Onco Targets Ther. 2019 Nov 19:12:9849-9860. doi: 10.2147/OTT.S227995. eCollection 2019.

Authors

Jia Hu¹, Youfang Chen¹, Xiaodong Li¹, Huikai Miao¹, Rongzhen Li¹, Dongni Chen¹, Zhesheng Wen¹

Affiliation

¹ Department of Thoracic Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou 510060, People's Republic of China.

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 (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.

Keywords: ONECUT2; THUMPD3-AS1; miR-543; non-small cell lung cancer; self-renewal.