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

## TL;DR

This study shows that circ_RPPH1 promotes bladder cancer growth and spread by interacting with EIF4A3 and enhancing EMT.

## Contribution

The paper reveals a novel mechanism by which circ_RPPH1 promotes bladder cancer progression via EIF4A3.

## Key findings

- High circ_RPPH1 levels correlate with deeper tumor invasion in bladder cancer.
- Circ_RPPH1 knockout reduces cancer cell proliferation, migration, and EMT.
- Circ_RPPH1 overexpression inhibits EIF4A3 binding to EMT-related mRNAs.

## Abstract

The involvement of circ_RPPH1 in bladder urothelial carcinoma (BUC) remains unclear, as well as the underlying mechanism.

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.

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.

Circ_RPPH1 promotes tumor growth and EMT in BUC by inhibiting EIF4A3-mediated mRNA regulation, activating the EIF4A3/N-cadherin/Vimentin pathway.

The online version contains supplementary material available at 10.1186/s41065-025-00442-3.