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BAP1-mediated ubiquitination inhibition and CAS6/AXL signaling activation in bladder cancer progression.

Liang Chen1, Zhenjun Liu2

  • 1Department of Urology Surgery, Feicheng People's Hospital, Tai'an, China.

Cytotechnology
|May 7, 2025
PubMed
Summary

BRCA1-associated protein 1 (BAP1) promotes bladder cancer by inhibiting SP1, YAP, and PD-L1 ubiquitination and activating CAS6/AXL signaling. BAP1 is a potential therapeutic target for bladder cancer.

Keywords:
BAP1Bladder cancerCAS6SP1Ubiquitination

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling Pathways

Background:

  • Bladder cancer progression is complex, involving dysregulated protein ubiquitination and signaling pathways.
  • BRCA1-associated protein 1 (BAP1) is implicated in various cellular processes, but its precise role in bladder cancer remains to be fully elucidated.
  • Understanding the regulatory mechanisms of key proteins like SP1, YAP, and PD-L1 is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of BAP1 in regulating the ubiquitination of SP1, YAP, and PD-L1 in bladder cancer.
  • To determine the impact of BAP1 on the CAS6/AXL signaling pathway and its contribution to bladder cancer progression.
  • To evaluate BAP1 as a potential therapeutic target for bladder cancer.

Main Methods:

  • Transcriptomic analysis of the GSE3167 dataset to identify gene expression patterns.
  • Establishment of a bladder cancer mouse model with BAP1 overexpression (OE-BAP1) and knockdown (KD-BAP1).
  • Western blot analysis, functional assays (scratch, Transwell, colony formation), and drug inhibition studies.

Main Results:

  • BAP1 overexpression significantly increased SP1, YAP, PD-L1, CAS6, AXL, and downstream signaling proteins (PI3K, STAT3, ERK½, MMP-2, MMP-9).
  • BAP1 knockdown decreased the levels of these proteins and inhibited bladder cancer cell migration, invasion, and proliferation.
  • Inhibition of SP1 or combined SP1 inhibition with anti-PD-L1 treatment effectively reduced cancer cell aggressiveness.

Conclusions:

  • BAP1 promotes bladder cancer progression by inhibiting the ubiquitination of SP1, YAP, and PD-L1.
  • BAP1 activates the CAS6/AXL signaling pathway, contributing to enhanced cell migration, invasion, and proliferation.
  • BAP1 represents a promising therapeutic target for bladder cancer treatment.