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lncRNA TUG1 Promotes Cell Proliferation, Migration, and Invasion in Hepatocellular Carcinoma via Regulating miR-29c-3p/COL1A1 Axis

Authors Zhao W, Jiang X, Yang S

Received 2 April 2020

Accepted for publication 14 July 2020

Published 4 August 2020 Volume 2020:12 Pages 6837—6847

DOI https://doi.org/10.2147/CMAR.S256624

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Antonella D'Anneo


Wei Zhao1 ,* Xue Jiang2 ,* Shuxia Yang2

1Department of Functional Examination, The Sixth People’s Hospital of Qingdao, Qingdao City, Shandong Province 266033, People’s Republic of China; 2Health Examination Center, The Sixth People’s Hospital of Qingdao, Qingdao City, Shandong Province 266033, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Shuxia Yang Tel +86-532-81636889
Email yangshuxia268@163.com

Background: Taurine upregulated gene 1 (TUG1) has been recognized as a novel oncogenic gene. The current study was established to explore the function and regulatory mechanism of TUG1 in hepatocellular carcinoma (HCC).
Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of TUG1, miR-29c-3p, and COL1A1 in tissues and cell lines. MTT assay, wound-healing and transwell assay were utilized for the detection of cell viability, migration and invasion, respectively. The interactions between miR-29c-3p and TUG1/COL1A1 were predicted by starBase v2.0 (http://starbase.sysu.edu.cn/) and verified by the dual-luciferase reporter or RNA immunoprecipitation assay. Western blot assay was performed to determine the protein levels of COL1A1, cyclin D1, E-cadherin, N-cadherin, Bcl-2, and Bax.
Results: Dramatically increased expression of TUG1 was noticed in HCC tissues and cell lines. TUG1 knockdown restrained the proliferation, migration, and invasion, and promoted the apoptosis of HCC cells. TUG1 targeted miR-29c-3p and inhibited miR-29c-3p expression. Overexpression of miR-29c-3p inhibited the proliferation, migration and invasion of HCC cells. MiR-29c-3p directly targeted COL1A1 and down-regulated COL1A1 expression. In addition, downregulation of miR-29c-3p and upregulation of COL1A1 both reversed the effects of TUG1 knockdown on the proliferation, apoptosis, migration, and invasion of HCC cells.
Conclusion: TUG1 could promote the proliferation, migration and invasion of HCC cells through regulating miR-29c-3p/COL1A1 axis. This novel finding might provide a latent target for the treatment of HCC.

Keywords: TUG1, miR-29c-3p, miR-29c-3p/COL1A1, hepatocellular carcinoma

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