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Restoration of UPK1A-AS1 Expression Suppresses Cell Proliferation, Migration, and Invasion in Esophageal Squamous Cell Carcinoma Cells Partially by Sponging microRNA-1248

Authors Du F, Guo T, Cao C

Received 20 November 2019

Accepted for publication 9 March 2020

Published 21 April 2020 Volume 2020:12 Pages 2653—2662

DOI https://doi.org/10.2147/CMAR.S239418

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Beicheng Sun


Fang Du,1 Tao Guo,2 Chenghua Cao3

1Department of Hematology and Oncology, No. 988 Hospital of Joint Logistic Support Force of the Chinese People’s Liberation Army, Zhengzhou, Henan Province, People’s Republic of China; 2Pediatric Intensive Care, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, People’s Republic of China; 3Translational Research Institute, Henan University, Kaifeng, Henan Province, People’s Republic of China

Correspondence: Fang Du
Department of Hematology and Oncology, No. 988 Hospital of Joint Logistic Support Force of the Chinese People’s Liberation Army, No. 602 Jianshe Road, Zhengzhou, Henan Province, People’s Republic of China
Email faex164@126.com

Background: Recent evidence suggests that long non-coding RNAs (lncRNAs) are emerging as key determinants of esophageal squamous cell carcinoma (ESCC) progression. This study aimed to investigate the role of lncRNA UPK1A antisense RNA 1 (UPK1A-AS1) in ESCC cell proliferation, invasion, and migration.
Methods: The expression levels of UPK1A-AS1 and miR-1248 were determined using quantitative reverse transcriptase-polymerase chain reaction. The functional role of UPK1A-AS1 in ESCC was investigated using subcellular localization assay, Cell Counting Kit-8 assay, colony formation assay, scratch-healing assay, and transwell invasion assay. The functional interaction between UPK1A-AS1 and miR-1248 was assessed using luciferase reporter and RNA pull-down assays.
Results: Twenty dysregulated lncRNAs were detected in ESCC. Downregulation of UPK1A-AS1 was observed in ESCC tissues and cell lines. Functionally, upregulation of UPK1A-AS1 suppressed the proliferation, migration, and invasion of ESCC cells. Moreover, an inverse correlation between UPK1A-AS1 and miR-1248 expression was observed in ESCC specimens, and miR-1248 was identified as a direct target of UPK1A-AS1. Furthermore, we found that UPK1A-AS1 exerts its anti-cancer effects partially through sponging miR-1248 in ESCC cells.
Conclusion: UPK1A-AS1 suppressed the proliferation, migration, and invasion of ESCC cells partially by sponging miR-1248. Hence, our findings provide novel insights into the regulatory pathway involved in ESCC development.

Keywords: esophageal squamous cell carcinoma, long non-coding RNA, UPK1A antisense RNA 1, miR-1248

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