已发表论文

UPK1A-AS1 表达恢复可抑制食管鳞状细胞癌的细胞增殖、迁移和侵袭,其中的部分作用来自微小 RNA-1248 海绵化

 

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

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




Figure 4 UPK1A-AS1 regulates ESCC cell proliferation, migration, and...