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Enhancement of Farnesoid X Receptor Inhibits Migration, Adhesion and Angiogenesis through Proteasome Degradation and VEGF Reduction in Bladder Cancers.

Authors
  • Lai, Chien-Rui1
  • Wang, Hisao-Hsien2
  • Chang, Hsin-Han1
  • Tsai, Yu-Ling3
  • Tsai, Wen-Chiuan3
  • Lee, Chen-Ray4
  • Changchien, Chih-Ying1, 5
  • Cheng, Yu-Chen1
  • Wu, Sheng-Tang6
  • Chen, Ying1
  • 1 Department of Biology and Anatomy, National Defense Medical Center, Taipei 11490, Taiwan. , (Taiwan)
  • 2 Department of Urology, Cheng Hsin General Hospital, Taipei 11490, Taiwan. , (Taiwan)
  • 3 Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan. , (Taiwan)
  • 4 Department of Medicine, National Defense Medical Center, Taipei 11490, Taiwan. , (Taiwan)
  • 5 Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan. , (Taiwan)
  • 6 Division of Urology, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan. , (Taiwan)
Type
Published Article
Journal
International Journal of Molecular Sciences
Publisher
MDPI AG
Publication Date
May 09, 2022
Volume
23
Issue
9
Identifiers
DOI: 10.3390/ijms23095259
PMID: 35563650
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

(1) Background: Bladder cancer is a malignant tumor mainly caused by exposure to environmental chemicals, with a high recurrence rate. NR1H4, also known as Farnesoid X Receptor (FXR), acts as a nuclear receptor that can be activated by binding with bile acids, and FXR is highly correlated with the progression of cancers. The aim of this study was to verify the role of FXR in bladder cancer cells. (2) Methods: A FXR overexpressed system was established to investigate the effect of cell viability, migration, adhesion, and angiogenesis in low-grade TSGH8301 and high-grade T24 cells. (3) Results: After FXR overexpression, the ability of migration, adhesion, invasion and angiogenesis of bladder cancer cells declined significantly. Focal adhesive complex, MMP2, MMP9, and angiogenic-related proteins were decreased, while FXR was overexpressed in bladder cancer cells. Moreover, FXR overexpression reduced vascular endothelial growth factor mRNA and protein expression and secretion in bladder cancer cells. After treatment with the proteosome inhibitor MG132, the migration, adhesion and angiogenesis caused by FXR overexpression were all reversed in bladder cancer cells. (4) Conclusions: These results may provide evidence on the role of FXR in bladder cancer, and thus may improve the therapeutic efficacy of urothelial carcinoma in the future.

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