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Circ_0000885 Enhances Osteosarcoma Progression by Increasing FGFR1 Expression via Sponging MiR-1294

Authors Chen Y, Zhang S, Bai C, Guan Z, Chen W

Received 31 December 2019

Accepted for publication 19 June 2020

Published 28 July 2020 Volume 2020:12 Pages 6441—6452


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Sanjeev Srivastava

Yinxian Chen, Sicheng Zhang, Chuanqing Bai, Zhiye Guan, Wenjian Chen

Department of Orthopedic, Children’s Hospital of Anhui Medical University, Hefei, Anhui 230032, People’s Republic of China

Correspondence: Wenjian Chen
Department of Orthopedic, Children’s Hospital of Anhui Medical University, Baohe District, Hefei, Anhui 230032, People’s Republic of China
Tel +86-13721021060

Background: As a malignant tumor, the progression of osteosarcoma (OS) is mediated by multiple regulators, including circular RNAs (circRNAs). However, the role of circ_0000885 in OS is unclear.
Materials and Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression of circ_0000885, miR-1294 and fibroblast growth factor receptor 1 (FGFR1). Cell proliferation was evaluated using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Flow cytometry and transwell assay were employed to determine the cell cycle distribution, cell migration and invasion, respectively. Moreover, the relationship between miR-1294 and circ_0000885 or FGFR1 was confirmed by dual-luciferase reporter assay. The protein level of FGFR1 was assessed via Western blot (WB) analysis. Animal experiments were used to verify the effect of circ_0000885 silencing on OS tumor growth in vivo.
Results: Circ_0000885 level was increased in OS tissues and cells. Knockdown of circ_0000885 repressed the proliferation, migration, invasion and induced cell cycle arrest in OS cells. There was a binding relationship between miR-1294 and circ_0000885, and miR-1294 inhibitor could reverse the inhibitory effect of silenced circ_0000885 on OS progression. MiR-1294 could target FGFR1, and overexpressed FGFR1 could invert the suppression effect of miR-1294 mimic on OS progression. Silencing of circ_0000885 hindered FGFR1 expression, while this effect could be recovered by miR-1294 inhibitor. In addition, circ_0000885 knockdown reduced OS tumor growth via regulating the FGFR1 expression by sponging miR-1294 in vivo.
Conclusion: Circ_0000885 played an active role in OS progression, indicating that it might be a potential target for OS therapy.

Keywords: OS, progression, circ_0000885, miR-1294, FGFR1

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