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Circular RNA circSPATA6 Inhibits the Progression of Oral Squamous Cell Carcinoma Cells by Regulating TRAF6 via miR-182

Authors Fan X, Wang Y

Received 13 November 2020

Accepted for publication 24 December 2020

Published 22 February 2021 Volume 2021:13 Pages 1817—1829

DOI https://doi.org/10.2147/CMAR.S292074

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Eileen O'Reilly


Xinhua Fan, Ying Wang

Department of Stomatology, Inner Mongolia Baotou Steel Hospital, Baotou City, Inner Mongolia, People’s Republic of China

Correspondence: Ying Wang Tel +86-472-5992490
Email wybaotou0812@126.com

Background: Oral squamous cell carcinoma (OSCC) has become a widely concerned social problem. Circular RNA spermatogenesis-associated protein 6 (circSPATA6) exhibited low expression in OSCC tissues, yet the regulatory mechanism of circSPATA6 remains vague.
Methods: Levels of circSPATA6, linear SPATA6, microRNA-182 (miR-182), and tumor necrosis factor receptor-associated factor 6 (TRAF6) were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Migration, invasion, cell cycle arrest, and apoptosis were assessed by Wound-healing, Matrigel invasion, and Flow cytometry assays. The binding relationship between miR-182 and circSPATA6 or TRAF6 was predicted by circRNA interactome or DIANA TOOL and then proved by the dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. TRAF6 protein level was measured by Western blot assay. The biological role of circSPATA6 on OSCC tumor growth was analyzed by xenograft tumor model in vivo. Exosomes were isolated and detected by differential centrifugation and a transmission electron microscope.
Results: CircSPATA6 and TRAF6 were declined, and miR-182 was elevated in OSCC cells. Functionally, circSPATA6 impeded migration and invasion, and facilitated cell cycle arrest and apoptosis of OSCC cells. Mechanistically, circSPATA6 could modulate TRAF6 expression through sponging miR-182. Moreover, circSPATA6 blocked tumor growth in the OSCC mice model. Exosomal circSPATA6 retarded the growth of OSCC cells.
Conclusion: CircSPATA6 curbed migration and invasion, and expedited cell cycle arrest and apoptosis in OSCC cells partly through regulating the miR-182/TRAF6 axis. These findings hinted at an underlying circRNA-targeted therapy for OSCC.

Keywords: circSPATA6, miR-182, TRAF6, oral squamous cell carcinoma

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