Journal
AGING-US
Volume 13, Issue 13, Pages 17673-17689Publisher
IMPACT JOURNALS LLC
Keywords
glioma; FOXM1; circRNA; circCCDC66; miR-320a
Categories
Funding
- National Natural Science Foundation of China [81201671]
- Foundation of Science and Technology Department of Jilin Province [20190101006JH, 20180101306JC, 20190201090JC]
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The study revealed that circCCDC66 acts as an oncogene in glioma by promoting cell proliferation, invasion and migration. CircCCDC66 was found to down-regulate miR-320a and up-regulate FOXM1, which in turn regulates multiple cancer-related pathways involved in DNA damage response. This suggests circCCDC66 may play a key role in glioma progression.
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.
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