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Research Paper|Volume 13, Issue 13|pp 17673—17689

Circular RNA circCCDC66 promotes glioma proliferation by acting as a ceRNA for miR-320a to regulate FOXM1 expression

Ling Qi1,2, Weiyao Wang1,2, Guifang Zhao1,3, Hong Jiang4, Yu Zhang5, Donghai Zhao3, Hong Jin3, Haiyang Xu6, Hongquan Yu6
  • 1The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan 511518, Guangdong, China
  • 2Department of Pathophysiology, Jilin Medical University, Jilin 132013, Jilin, China
  • 3Department of Pathology, Jilin Medical University, Jilin 132013, Jilin, China
  • 4Department of Ophthalmology, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China
  • 5Department of Neurovascular, First Hospital of Jilin University, Changchun 130021, Jilin, China
  • 6Department of Oncological Neurosurgery, First Hospital of Jilin University, Changchun 130021, Jilin, China
Received: November 17, 2020Accepted: May 11, 2021Published: July 12, 2021
https://doi.org/10.18632/aging.203258

Copyright: © 2021 Qi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: In this study, we determine the potential roles and uncover the regulatory mechanisms of circCCDC66 in regulating cell growth and cell metastasis of glioma.

Methods: qRT-PCR was used to detect the expressions of circCCDC66 in gliomas and tissues. The biological function of circCCDC66 in glioma cell lines was elucidated by functional experiments. Cell counting kit-8 and transwell were used to detect the effect of circCCDC66 on the proliferation, migration and invasion of glioma cells. Bioinformatics analysis was applied to reveal the targets of circCCDC66.

Results: The results showed circCCDC66 was overexpressed in glioma and acted as an oncogene. CircCCDC66 knockdown suppressed the proliferation, migration, and invasion of glioma cells. We constructed a circCCDC66 regulating miRNA network and revealed miR-320a was a potential target of circCCDC66, which was down-regulated in high-grade gliomas compared to low-grade gliomas. Bioinformatics analysis showed circCCDC66-miR-320a/b axis was involved in regulating multiple cancer-related pathways. Furthermore, we identified FOXM1 as a key target of circCCDC66, which was involved in regulating DNA damage response pathways. In mechanism study, circCCDC66 could sponge miR-320a, thereby increasing the expression of FOXM1.

Conclusions: CircCCDC66 could facilitate glioma cells proliferation, invasion and migration by down-regulating miR-320a and up-regulating FOXM1.