MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway
Authors Liu L, Jiang H, Zhao J, Wen H
Received 12 October 2017
Accepted for publication 7 February 2018
Published 23 August 2018 Volume 2018:11 Pages 5111—5119
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 2
Editor who approved publication: Dr Tohru Yamada
Lijun Liu,1,2 Han Jiang,3 Jin Zhao,3 Hao Wen2
1Department of Stomatology, Stomatology of Mylike Plastic and Cosmetic Hospital of ChongQing, Chongqing, China; 2Department of Oral and Maxillofacial Surgery, School of Stomatology, The First Affiliated Hospital of Xinjiang Medical University, Xinjiang, China; 3Department of Periodontics, School of Stomatology, The First Affiliated Hospital of Xinjiang Medical University, Xinjiang, China
Background: Oral carcinoma, one of the most commonly diagnosed cancers, has a poor prognosis and low survival rate with treatment. In recent years, some studies reported the upregulation of miRNA-16 (miR-16) in the oral carcinoma, whereas some other studies confirmed the downregulation of miR-16. In the current study, we aimed to investigate the function of miR-16 in oral carcinoma.
Materials and methods: Cell proliferation assay was measured by MTT assay, quantitative real time polymerase chain reaction (qRT-PCR) was used to evaluate the expression of miR-16, and apoptosis was analyzed by flow cytometry. In addition, the expression of proteins was detected by Western blot. Moreover, xenograft tumor model was established to detect the effect of miR-16 in vivo.
Results: The results suggested that miR-16 was downregulated in the oral carcinoma tissues. Overexpression of miR-16 inhibited the growth and proliferation of oral squamous carcinoma cells (OSCCs) and induced apoptosis both in vitro and in vivo, which is due to the suppression of Wnt/β-catenin signaling pathway.
Conclusion: This study provides evidence that overexpression of miR-16 inhibits OSCC growth by regulating Wnt/β-catenin signaling. Our findings suggest that overexpression of miR-16 could be a potential approach for gene therapy of OSCC in future.
Keywords: oral carcinoma, miRNA-16, apoptosis, Wnt/β-catenin signaling
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