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CircGDI2 Regulates the Proliferation, Migration, Invasion and Apoptosis of OSCC via miR-454-3p/FOXF2 Axis

Authors Shi D, Li H, Zhang J, Li Y

Received 14 August 2020

Accepted for publication 10 December 2020

Published 11 February 2021 Volume 2021:13 Pages 1371—1382


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Seema Singh

Dan Shi,1 Huiyun Li,2 Junge Zhang,3 Yadong Li1

1Department of Oral Medicine Centre, Henan Provincial People’s Hospital, Zhengzhou, Henan, People’s Republic of China; 2Department of Anesthesiology, Henan Provincial People’s Hospital, Zhengzhou, Henan, People’s Republic of China; 3Department of Ophthalmology, Henan Provincial People’s Hospital, Zhengzhou, Henan, People’s Republic of China

Correspondence: Yadong Li
Department of Oral Medicine Centre, Henan Provincial People’s Hospital, No. 7 Wei-Wu Road, Zhengzhou City, 450000 Henan Province, People’s Republic of China
Tel +86-186-38723618

Background: Aberrant expression of circular RNA (circRNA) is involved in the occurrence and development of multifarious cancers, including oral squamous cell carcinoma (OSCC). However, the biological role of circGDI2 and the action mechanism in OSCC remain largely unclear.
Methods: The expression levels of circGDI2, miR-454-3p and forkhead box F2 (FOXF2) were examined by quantitative real-time PCR (qRT-PCR) or Western blot. The stability of circGDI2 was confirmed by Ribonuclease R (RNase R) assay. Cell Counting Kit 8 (CCK8) assay, colony formation and transwell assay were used to detect cell proliferation, migration or invasion. Cell apoptosis was tested by flow cytometry. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were employed to verify the interaction between miR-454-3p and circGDI2 or FOXF2. Moreover, xenograft mouse models were constructed to assess tumor growth in vivo.
Results: CircGDI2 was a stable circRNA and was low expressed in OSCC tissues and cells. CircGDI2 overexpression could effectively inhibit the proliferation, migration, invasion and promote apoptosis in OSCC cells, and suppress OSCC tumor growth in nude mice in vivo. MiR-454-3p could be sponged by circGDI2, and its overexpression could mitigate the suppressive effects of circGDI2 overexpression on OSCC progression. In addition, FOXF2 was a target of miR-454-3p, and miR-454-3p silence could impede the cell growth of OSCC cells by enhancing FOXF2 expression. Meanwhile, circGDI2 positively regulated FOXF2 expression by targeting miR-454-3p.
Conclusion: CircGDI2 served as a repressor to restrain OSCC malignancy via miR-454-3p/FOXF2 axis, which might be a novel biomarker for targeted OSCC therapy.

Keywords: OSCC, circGDI2, miR-454-3p, FOXF2

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