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Circ_0000517 Contributes to Hepatocellular Carcinoma Progression by Upregulating TXNDC5 via Sponging miR-1296-5p

Authors Zang H, Li Y, Zhang X, Huang G

Received 28 December 2019

Accepted for publication 17 April 2020

Published 14 May 2020 Volume 2020:12 Pages 3457—3468


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Antonella D'Anneo

Hongliang Zang, Yuhui Li, Xue Zhang, Guomin Huang

Department of General Surgery, China-Japan Union Hospital of Jilin University, Jilin, Changchun 130012, People’s Republic of China

Correspondence: Guomin Huang
Department of General Surgery, China-Japan Union Hospital of Jilin University, No. 829 Xinmin Street, Jilin, Changchun 130012, People’s Republic of China
Tel +86-431-84997753

Background: Circular RNAs (circRNAs) function as essential regulators in diverse human cancers, including hepatocellular carcinoma (HCC). However, the function of circ_0000517 in HCC was unknown. We aimed to explore the roles and mechanisms of circ_0000517 in HCC.
Materials and Methods: The levels of circ_0000517, RPPH1 mRNA and microRNA-1296-5p (miR-1296-5p) were measured using quantitative real-time polymerase chain reaction (qRT-PCR). The characteristics of circ_0000517 were explored by RNase R digestion and actinomycin D assays. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell cycle process and cell apoptosis were analyzed by flow cytometry analysis. The function of circ_0000517 in vivo was explored by a murine xenograft model. The association between miR-1296-5p and circ_0000517 or thioredoxin domain containing 5 (TXNDC5) was determined by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The protein level of TXNDC5 was detected by Western blot assay.
Results: Circ_0000517 was upregulated in HCC tissues and cells. Silencing of circ_0000517 suppressed HCC cell viability and colony formation and promoted cell cycle arrest and apoptosis in vitro and hampered tumor growth in vivo. MiR-1296-5p was a target of circ_0000517 and the effects of circ_0000517 silencing on HCC cell viability, cell cycle, colony formation and apoptosis were abolished by miR-1296-5p inhibition. TXNDC5 functioned as a target gene of miR-1296-5p, and the inhibitory effect of miR-1296-5p on HCC cell progression was rescued by TXNDC5 overexpression. Moreover, circ_0000517 promoted TXNDC5 expression via targeting miR-1296-5p.
Conclusion: Circ_0000517 accelerated HCC progression by upregulating TXNDC5 through sponging miR-1296-5p.

Keywords: HCC, circ_0000517, miR-1296-5p, TXNDC5

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