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Downregulated RBM5 Enhances CARM1 Expression and Activates the PRKACA/GSK3β Signaling Pathway through Alternative
Yanping Zhang1, Fang Li2, Zhenwei Han1
1Department of Urology, The Second Hospital of Hebei Medical University, Shijiazhuang 050011, China.
Cancers
|January 11, 2024
Summary
Downregulated RNA-binding motif protein 5 (RBM5) accelerates bladder cancer by increasing coactivator-associated arginine methyltransferase 1 (CARM1) expression. This study reveals RBM5
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- RNA-binding motif protein 5 (RBM5) downregulation is linked to tumor progression, including bladder cancer (BC).
- Alternative splicing (AS) and nonsense-mediated mRNA decay (NMD) are implicated in cancer progression.
- The specific role of RBM5 in BC via AS-NMD pathways is not well understood.
Purpose of the Study:
- To investigate the role of RBM5 in bladder cancer progression.
- To elucidate the mechanism by which RBM5 influences bladder cancer through alternative splicing and NMD.
- To identify potential therapeutic targets for bladder cancer.
Main Methods:
- Analyzing RBM5 expression in BC cells and tissues.
- Investigating the interaction between RBM5 and CARM1 mRNA.
- Assessing the impact of RBM5 on the Wnt/β-catenin pathway.
- Examining the role of PRKACA in BC progression.
Main Results:
- RBM5 downregulation increased coactivator-associated arginine methyltransferase 1 (CARM1) expression in BC.
- CARM1 activation of the Wnt/β-catenin axis promoted BC cell proliferation and poor prognosis.
- RBM5 directly binds CARM1 mRNA, mediating AS-NMD to reduce CARM1 levels.
- PRKACA, regulated by CARM1, promotes BC growth.
Conclusions:
- A novel RBM5/CARM1/PRKACA regulatory axis controlling Wnt/β-catenin activation in BC was identified.
- RBM5 functions to suppress BC progression by downregulating CARM1 via AS-NMD.
- This axis represents a potential therapeutic target for bladder cancer treatment.
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