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miR-381 Mediates the Development of Head and Neck Squamous Cell Carcinoma via Targeting STC2

Authors Ma HF, Lv GX, Zhang DH

Received 16 January 2020

Accepted for publication 28 April 2020

Published 21 May 2020 Volume 2020:13 Pages 4485—4493

DOI https://doi.org/10.2147/OTT.S246289

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Yao Dai


Hai-Feng Ma, Guo-Xiao Lv, Da-Hai Zhang

Department of Radiotherapy, Zhejiang Dongyang People’s Hospital, Dongyang 322100, Zhejiang Province, People’s Republic of China

Correspondence: Da-Hai Zhang
Department of Radiotherapy, Zhejiang Dongyang People’s Hospital, No. 60 West Wuning Road, Dongyang 322100, Zhejiang Province, People’s Republic of China
Tel +86-13819938996
Email seazhang_dy@163.com

Objective: miR-381 is implicated in the occurrence and development of various cancers, yet its role in head and neck squamous cell carcinoma (HNSCC) remains largely unknown. This study sought to research the direct target of miR-381 in HNSCC and investigate their roles in cancer progression.
Methods: miRNA and mRNA expression files of HNSCC were accessed from TCGA database and then processed for differential analysis. Bioinformatics databases were employed to predict the target mRNAs of the potential miRNA. qRT-PCR was conducted to determine the expression levels of the target miRNA and mRNA. Then, a series of in vitro experiments like CCK-8, colony formation assay, wound healing assay and transwell assay were performed to detect cell proliferation, migration and invasion. Dual-luciferase reporter gene assay was carried out for the further validation of the targeted relationship between the miRNA and mRNA.
Results: miR-381 was observed to be greatly down-regulated in HNSCC cells, and its overexpression could inhibit cell proliferation, migration and invasion. Besides, dual-luciferase reporter gene assay confirmed that STC2 was a direct target of miR-381, and their expression levels were reversely correlated. Moreover, rescue experiments demonstrated that overexpressing STC2 could rescue the inhibitory effect of miR-381 overexpression on cell proliferation, migration and invasion. Also, we verified that miR-381/STC2 exerted its function on HNSCC proliferation by mediating the FAK/PI3K/Akt/mTOR signaling pathway.
Conclusion: miR-381 suppresses cell proliferation, migration and invasion in HNSCC through targeting STC2, and participates in HNSCC development probably via the FAK/PI3K/Akt/mTOR signaling pathway.

Keywords: miR-381, STC2, FAK/PI3K/Akt/mTOR, HNSCC

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