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Long Non-Coding RNA CASC19 Sponges microRNA-532 and Promotes Oncogenicity of Clear Cell Renal Cell Carcinoma by Increasing ETS1 Expression

Authors Luo Y, Liu F, Yan C, Qu W, Zhu L, Guo Z, Zhou F, Zhang W

Received 15 December 2019

Accepted for publication 27 February 2020

Published 24 March 2020 Volume 2020:12 Pages 2195—2207


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Eileen O'Reilly

Yu Luo, Feng Liu, Chunhui Yan, Wei Qu, Liang Zhu, Zheng Guo, Fan Zhou, Wei Zhang

Department of Urology, The 161st Hospital of the People’s Liberation Army, Wuhan, Hubei 430010, People’s Republic of China

Correspondence: Feng Liu
Department of Urology, The 161st Hospital of the People’s Liberation Army, No. 68, Huangpu Road, Wuhan, Hubei 430010, People’s Republic of China

Purpose: The long non-coding RNA cancer susceptibility 19 (CASC19) is recognized as an important regulator in gastric cancer, colorectal cancer, and non-small cell lung cancer. Nevertheless, to the best of our knowledge, the expression status and detailed roles of CASC19 in clear cell renal cell carcinoma (ccRCC) have not been elucidated. Hence, we aimed to determine CASC19 expression in ccRCC and investigate its roles in ccRCC oncogenicity. The molecular mechanisms underlying CASC19 functions in ccRCC were also determined.
Methods: CASC19 expression was measured by using reverse transcription-quantitative polymerase chain reaction. The effects of CASC19 on ccRCC cell proliferation, colony formation, migration, and invasiveness in vitro, as well as on tumor growth in vivo, were examined by the MTT assay, colony formation assay, cell migration and invasiveness assays, and tumor xenograft in nude nice, respectively.
Results: CASC19 was overexpressed in ccRCC tissues and cell lines. High expression of CASC19 was closely associated with unfavorable clinicopathological parameters and predicted negative clinical outcomes in patients with ccRCC. Knockdown of CASC19 decreased ccRCC cell proliferation, colony formation, migration, and invasiveness, as well as attenuated tumor growth in vivo. Mechanistically, CASC19 functioned as a competing endogenous RNA and upregulated the expression of ETS proto-oncogene 1 (ETS1) through sponging microRNA-532 (miR-532). Furthermore, rescue assays revealed that inhibiting miR-532 or restoring ETS1 expression partially abolished the impacts of CASC19 knockdown on ccRCC cells.
Conclusion: The CASC19/miR-532/ETS1 regulatory pathway is crucial for the malignant manifestations of ccRCC, which makes it an attractive target for potential treatments of ccRCC.

Keywords: cancer, MTT assay, cell migration, invasiveness, xenograft, knockdown

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