CircDOCK1 Regulates miR-186/DNMT3A to Promote Osteosarcoma Progression
Background: Circular RNAs (circRNAs), as a class of endogenous RNAs, are implicated in osteosarcoma (OS) progression. However, the functional properties of circDOCK1 in OS have been largely unexplored. The present study demonstrated the regulatory mechanism of circDOCK1 in OS. Methods: QRT-PCR and W...
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| Format: | Article |
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MDPI AG
2022-11-01
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| Series: | Biomedicines |
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| Online Access: | https://www.mdpi.com/2227-9059/10/12/3013 |
| _version_ | 1797461345840398336 |
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| author | Zhihui Jin Jia Ye Sen Chen Yijun Ren Weichun Guo |
| author_facet | Zhihui Jin Jia Ye Sen Chen Yijun Ren Weichun Guo |
| author_sort | Zhihui Jin |
| collection | DOAJ |
| description | Background: Circular RNAs (circRNAs), as a class of endogenous RNAs, are implicated in osteosarcoma (OS) progression. However, the functional properties of circDOCK1 in OS have been largely unexplored. The present study demonstrated the regulatory mechanism of circDOCK1 in OS. Methods: QRT-PCR and Western blots were used to determine the abundances of circDOCK1, miR-186, and DNMT3A. Cell counting kit-8 (CCK-8), 5-Ethynyl-2′-deoxyuridine (EdU), colony formation, Transwell, and wound healing assays were used to examine cellular multiplication, motility, and invasion. Luciferase reporter analysis, RNA immunoprecipitation (RIP), and pull-down assays were used to verify target relationships. Xenograft models were used to analyze in vivo function. Results: OS tissues and cells showed high levels of circDOCK1. By knocking down circDOCK1, cellular multiplication, motility, and invasion were suppressed. Furthermore, silencing circDOCK1 suppressed the growth of tumor xenografts. According to mechanistic studies, miR-186 targets DNA methyltransferases 3A (DNMT3A) directly and acts as a circDOCK1 target. Furthermore, circDOCK1 upregulated DNMT3A expression through sponging miR-186 to regulate the progression of OS. Conclusions: CircDOCK1 promotes OS progression by interacting with miR-186/DNMT3ADNMT3A, representing a novel therapeutic approach. |
| first_indexed | 2024-03-09T17:18:06Z |
| format | Article |
| id | doaj.art-4aee2fd8f72949e2a717e201b2890221 |
| institution | Directory Open Access Journal |
| issn | 2227-9059 |
| language | English |
| last_indexed | 2024-03-09T17:18:06Z |
| publishDate | 2022-11-01 |
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| spelling | doaj.art-4aee2fd8f72949e2a717e201b28902212023-11-24T13:25:11ZengMDPI AGBiomedicines2227-90592022-11-011012301310.3390/biomedicines10123013CircDOCK1 Regulates miR-186/DNMT3A to Promote Osteosarcoma ProgressionZhihui Jin0Jia Ye1Sen Chen2Yijun Ren3Weichun Guo4Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan 430060, ChinaDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan 430060, ChinaDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan 430060, ChinaDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan 430060, ChinaDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan 430060, ChinaBackground: Circular RNAs (circRNAs), as a class of endogenous RNAs, are implicated in osteosarcoma (OS) progression. However, the functional properties of circDOCK1 in OS have been largely unexplored. The present study demonstrated the regulatory mechanism of circDOCK1 in OS. Methods: QRT-PCR and Western blots were used to determine the abundances of circDOCK1, miR-186, and DNMT3A. Cell counting kit-8 (CCK-8), 5-Ethynyl-2′-deoxyuridine (EdU), colony formation, Transwell, and wound healing assays were used to examine cellular multiplication, motility, and invasion. Luciferase reporter analysis, RNA immunoprecipitation (RIP), and pull-down assays were used to verify target relationships. Xenograft models were used to analyze in vivo function. Results: OS tissues and cells showed high levels of circDOCK1. By knocking down circDOCK1, cellular multiplication, motility, and invasion were suppressed. Furthermore, silencing circDOCK1 suppressed the growth of tumor xenografts. According to mechanistic studies, miR-186 targets DNA methyltransferases 3A (DNMT3A) directly and acts as a circDOCK1 target. Furthermore, circDOCK1 upregulated DNMT3A expression through sponging miR-186 to regulate the progression of OS. Conclusions: CircDOCK1 promotes OS progression by interacting with miR-186/DNMT3ADNMT3A, representing a novel therapeutic approach.https://www.mdpi.com/2227-9059/10/12/3013circDOCK1miR-186DNMT3AOSprogression |
| spellingShingle | Zhihui Jin Jia Ye Sen Chen Yijun Ren Weichun Guo CircDOCK1 Regulates miR-186/DNMT3A to Promote Osteosarcoma Progression Biomedicines circDOCK1 miR-186 DNMT3A OS progression |
| title | CircDOCK1 Regulates miR-186/DNMT3A to Promote Osteosarcoma Progression |
| title_full | CircDOCK1 Regulates miR-186/DNMT3A to Promote Osteosarcoma Progression |
| title_fullStr | CircDOCK1 Regulates miR-186/DNMT3A to Promote Osteosarcoma Progression |
| title_full_unstemmed | CircDOCK1 Regulates miR-186/DNMT3A to Promote Osteosarcoma Progression |
| title_short | CircDOCK1 Regulates miR-186/DNMT3A to Promote Osteosarcoma Progression |
| title_sort | circdock1 regulates mir 186 dnmt3a to promote osteosarcoma progression |
| topic | circDOCK1 miR-186 DNMT3A OS progression |
| url | https://www.mdpi.com/2227-9059/10/12/3013 |
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