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Long Non-Coding RNA TRIM52-AS1 Promotes Growth and Metastasis via miR-218-5p/ROBO1 in Hepatocellular Carcinoma

Authors Liu Y, Wu Y, Liu S, Dai Y

Received 13 October 2020

Accepted for publication 26 December 2020

Published 22 January 2021 Volume 2021:13 Pages 547—558

DOI https://doi.org/10.2147/CMAR.S286205

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Xueqiong Zhu


Yuanjun Liu,* Yakun Wu,* Shuang Liu, Yi Dai

Department of Hepatobiliary Surgery, Suining Central Hospital, Suining 629000, Sichuan Province, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Yi Dai
Department of Hepatobiliary Surgery, Suining Central Hospital, No. 127 Desheng West Road, Chuanshan District, Suining 629000, Sichuan Province, People’s Republic of China
Email 158650601@qq.com

Background: Hepatocellular carcinoma (HCC) is a malignant disease with a high mortality among primary HCC patients worldwide. Lots of studies have shown that lncRNAs are known as the biomarkers in diagnosis, treatment and prognosis of hepatocellular carcinoma. Therefore, clarifying the detailed function and mechanism of the lncRNA in the HCC progressing seems particularly important.
Methods: The TCGA and GEO database and RT-qPCR were used to analyse the expression of TRIM52-AS1 in HCC tissues and cell lines. Clinical data were collected to further analyze the correlation between indicators of clinical samples and the expression of TRIM52-AS1. CCK-8, plate clone and transwell assays were employed to evaluate the role of TRIM52-AS1 on cell proliferation, migration and invasion. Then, bioinformatics prediction, luciferase reporter, RNA immunoprecipitation (RIP), and RT-qPCR were employed to analyze the direct interaction among TRIM52-AS1, miR-218-5p and ROBO1. Additionally, the rescue function assays were used to verify that miR-218-5p/ROBO1 was the function downstream of TRIM52-AS1.
Results: TRIM52-AS1 was overexpressed in HCC according to the TCGA database and RT-qPCR assay. The expression of TRIM52-AS1 was higher in the metastatic foci compared with primary tumor according to the GEO database. Additionally, TRIM52-AS1 knockdown inhibited the proliferation and metastasis of HCC cells. TRIM52-AS1 could act as competitive endogenous RNA to regulate ROBO1 through miR-218-5p, then promoted the HCC cell progression.
Conclusion: TRIM52-AS1 is overexpressed in HCC and can promote the proliferation and metastasis of HCC cells through miR-218-5p/ROBO1 axis, then drives the HCC cell progression.

Keywords: TRIM52-AS1, ROBO1, miR-218-5p, hepatocellular carcinoma, growth, metastasis

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