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
- 1 The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan 511518, Guangdong, China
- 2 Department of Pathophysiology, Jilin Medical University, Jilin 132013, Jilin, China
- 3 Department of Pathology, Jilin Medical University, Jilin 132013, Jilin, China
- 4 Department of Ophthalmology, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China
- 5 Department of Neurovascular, First Hospital of Jilin University, Changchun 130021, Jilin, China
- 6 Department of Oncological Neurosurgery, First Hospital of Jilin University, Changchun 130021, Jilin, China
Received: November 17, 2020 Accepted: May 11, 2021 Published: July 12, 2021https://doi.org/10.18632/aging.203258
How to Cite
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.
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.