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Long non-coding RNA LINC00662 promotes proliferation and migration in oral squamous cell carcinoma

Authors Xu D, Chen Y, Yuan C, Zhang S, Peng W

Received 25 September 2018

Accepted for publication 3 January 2019

Published 18 January 2019 Volume 2019:12 Pages 647—656

DOI https://doi.org/10.2147/OTT.S188691

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 3

Editor who approved publication: Dr Tohru Yamada


Debin Xu,1,* Yunmei Chen,2,* Chunlei Yuan,3 Shuyong Zhang,1 Wei Peng2

1Department of Thyroid and Neck Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People’s Republic of China; 2Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, People’s Republic of China; 3Department of Breast Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People’s Republic of China

*These authors contributed equally to this work

Background: Although increasing evidence has demonstrated important roles for long non-coding RNAs (lncRNAs) in cancer development, their functions in oral squamous cell carcinoma (OSCC) growth remain largely unknown. Therefore, we aimed to investigate the role of LINC00662 in OSCC.
Methods: The expression of LINC00662 in 61 OSCC tissues and four OSCC cell lines were detected by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Cell proliferation was detected using Cell Counting Kit-8 (CCK-8) and EdU staining methods. Migration and invasion abilities were analyzed using transwell and wound healing assay. Cell cycle distribution and apoptosis rate were evaluated by flow cytometry. Western blot method was performed to detect protein expression.
Results: We found that the expression of LINC00662 was significantly increased in OSCC tissues, and a higher expression of LINC00662 was detected in larger tumor size, higher stage tumors and with lymph node metastasis. Moreover, overexpression of LINC00662 induced OSCC cell proliferation, increased migration and invasion abilities, and suppressed cell apoptosis. Knockdown of LINC00662 decreased the proliferation, migration, and invasion abilities of OSCC cell, and induced apoptosis. Furthermore, LINC00662 regulated the Wnt/β-catenin pathway.
Conclusion: Our data indicate that LINC00662 may represent a novel indicator of OSCC and may be a potential therapeutic target for diagnosis and therapy.

Keywords: LINC00662, proliferation, migration, Wnt/β-catenin pathway, OSCC


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