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LncRNA HCG18 Promotes Clear Cell Renal Cell Carcinoma Progression by Targeting miR-152-3p to Upregulate RAB14

Authors Yang Y, Gong P, Yao D, Xue D, He X

Received 22 December 2020

Accepted for publication 31 January 2021

Published 11 March 2021 Volume 2021:13 Pages 2287—2294

DOI https://doi.org/10.2147/CMAR.S298649

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Ahmet Emre Eşkazan


Yu Yang,1 Pengfeng Gong,2 Dongwei Yao,3 Dong Xue,2 Xiaozhou He2

1Department of Hepatopancreatobiliary Surgery, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, People’s Republic of China; 2Department of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, People’s Republic of China; 3Department of Urology, The Second People’s Hospital of Lianyungang, Lianyungang, Jiangsu, People’s Republic of China

Correspondence: Xiaozhou He
Department of Urology, The Third Affiliated Hospital of Soochow University, No. 185, Juqian Road, Changzhou, 213000, People’s Republic of China
Tel +86-519-68873211
Email [email protected]

Background: Long noncoding RNAs (lncRNAs) have been regarded as crucial regulators in many cancers, including clear cell renal cell carcinoma (ccRCC). This research aimed to explore the biological role and molecular mechanism of lncRNA HCG18 in ccRCC.
Materials and Methods: The expression levels of HCG18, miR-152-3p and RAB14 were examined by RT-qPCR. Cell viability, migration and invasion were examined by CCK-8 and transwell assays. Luciferase reporter and RIP assays were adopted to verify the interaction between miR-152-3p and HCG18 or RAB14.
Results: It was found that HCG18 expression was highly expressed in ccRCC tissues and cells, and patients with high expression of HCG18 had a short overall survival time. Moreover, HCG18 depletion attenuated ccRCC cell viability, migration and invasion. In addition, miR-152-3p was confirmed as a downstream target of HCG18 and was inversely regulated by HCG18, and RAB14 was a target of miR-152-3p. Functional assays demonstrated that miR-152-3p silencing or RAB14 addition abolished the inhibitory effects of HCG18 knockdown on ccRCC progression.
Conclusion: The results of the present study indicated that HCG18 accelerated the development and progression of ccRCC by upregulating RAB14 via sponging miR-152-3p, suggesting a potential therapeutic target for patients with ccRCC.

Keywords: HCG18, miR-152-3p, RAB14, clear cell renal cell carcinoma

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