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Background <p>The involvement of circ_RPPH1 in bladder urothelial carcinoma (BUC) remains unclear, as well as the underlying mechanism.</p> Methods <p>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.</p> Results <p>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.</p> Conclusion <p>Circ_RPPH1 promotes tumor growth and EMT in BUC by inhibiting EIF4A3-mediated mRNA regulation, activating the EIF4A3/N-cadherin/Vimentin pathway.</p>

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Circ_RPPH1 promotes bladder urothelium carcinoma proliferation and EMT by recruiting and binding to EIF4 A3

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月9日

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  • HuaWei Liu,
  • JunMin Ma,
  • Xia Yan

摘要

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.