Long noncoding RNA Sox2 overlapping transcript (SOX2OT) promotes non-small-cell lung cancer migration and invasion via sponging microRNA 132 (miR-132)
Authors Zhang K, Li Y, Qu L, Ma X, Zhao H, Tang Y
Received 19 March 2018
Accepted for publication 25 May 2018
Published 30 August 2018 Volume 2018:11 Pages 5269—5278
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr William Cho
Kewei Zhang,1,* Yang Li,2,* Limei Qu,3 Xiaobo Ma,3 Hongguang Zhao,4 Ying Tang2
1Department of Thoracic surgery, The First Hospital of Jilin University, Changchun 130021, People’s Republic of China; 2Department of Respiration, The First Hospital of Jilin University, Changchun 130021, People’s Republic of China; 3Department of Pathology, The First Hospital of Jilin University, Changchun 130021, People’s Republic of China; 4Department of Nuclear Medicine, The First Hospital of Jilin University, Changchun 130021, People’s Republic of China
*These authors contributed equally to this work
Background: Long noncoding RNA (lncRNA) Sox2 overlapping transcript (SOX2OT) has been reported to be upregulated in various types of cancers, including non-small-cell lung cancer (NSCLC). However, the biological role and underlying mechanism of SOX2OT activity in NSCLC remain largely unknown. This study aims to investigate the function and possible molecular mechanisms of SOX2OT in NSCLC.
Materials and methods: Quantitative real-time polymerase chain reaction was used to detect SOX2OT expression, and cellular proliferation, migration, and invasion were measured using cell counting kit-8, wound healing, and Transwell invasion assays, respectively. Western blotting was used to determine protein expression. Starbase 2.0 and luciferase reporter assay were utilized to identify the molecular target of SOX2OT.
Results: Here, we discovered that SOX2OT was markedly upregulated in NSCLC tissues and cell lines. Knockdown of SOX2OT inhibited the proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) process in NSCLC cells. Moreover, we explored the regulatory mechanism of SOX2OT and found that SOX2OT directly bound microRNA 132 (miR-132) in NSCLC cells. Importantly, miR-132 inhibition partially reversed the SOX2OT knockdown-mediated inhibitory effect on cell proliferation, migration, invasion, and EMT process. We also found that SOX2OT could regulate zinc finger E-box-binding homeobox 2 (a target of miR-132) expression, which played crucial roles in tumor cell proliferation and invasion.
Conclusion: These findings indicated that SOX2OT was a noncoding oncogene that exerted important regulatory functions in NSCLC via sponging miR-132 and might represent a novel strategy for overcoming this disease.
Keywords: non-small-cell lung cancer, SOX2OT, miR-132, ZEB2
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