Circ_RPPH1 promotes bladder urothelium carcinoma proliferation and EMT by recruiting and binding to EIF4 A3
Abstract Background The involvement of circ_RPPH1 in bladder urothelial carcinoma (BUC) remains unclear, as well as the underlying mechanism. Methods Circ_RPPH1 levels in BUC cells and tissues were measured via RT-qPCR. Downregulation of circ_RPPH1 was assessed using colony formation, CCK-8, wound h...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2025-05-01
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| Series: | Hereditas |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s41065-025-00442-3 |
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| Summary: | Abstract Background The involvement of circ_RPPH1 in bladder urothelial carcinoma (BUC) remains unclear, as well as the underlying mechanism. Methods Circ_RPPH1 levels in BUC cells and tissues were measured via RT-qPCR. Downregulation of circ_RPPH1 was assessed using colony formation, CCK-8, wound healing, and Transwell assays to evaluate proliferation, migration, and invasion. RIP and RNA pull-down confirmed circ_RPPH1 binding to EIF4A3, while immunoblotting analyzed EIF4A3 and EMT-related proteins. Results High circ_RPPH1 levels in BUC correlated with tumor invasion depth. Its knockout suppressed proliferation, invasion, and EMT, while circ_RPPH1 overexpression reduced EIF4A3 binding to N-cadherin and Vimentin mRNA, promoting EMT. Conclusion Circ_RPPH1 promotes tumor growth and EMT in BUC by inhibiting EIF4A3-mediated mRNA regulation, activating the EIF4A3/N-cadherin/Vimentin pathway. |
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| ISSN: | 1601-5223 |