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WNT7B represses epithelial-mesenchymal transition and stem-like properties in bladder urothelial carcinoma

Lei Na1, Zhuo Wang2, Yu Bai3

  • 1Department of Pathophysiology, College of Basic Medical Science, China Medical University, Shenyang, China; Department of Urology, Shengjing Hospital of China Medical University, Shenyang, China.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|September 25, 2021
PubMed
Abstract

Insights

WNT7B acts as a tumor suppressor in bladder cancer by inhibiting cell stemness, EMT, and chemoresistance. This pathway, involving FZD5, ELF3, and NOTCH1, offers a new target for bladder urothelial carcinoma treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Recurrence and metastasis are critical challenges in bladder urothelial carcinoma.
  • Tumor cell stemness, epithelial-mesenchymal transition (EMT), and chemoresistance contribute significantly to these issues.

Purpose of the Study:

  • To investigate the role of WNT7B in bladder urothelial carcinoma.
  • To elucidate the signaling pathway involving WNT7B, FZD5, ELF3, and NOTCH1.

Main Methods:

  • Analysis of TCGA and CCLE databases for gene expression.
  • Immunohistochemistry on patient specimens.
  • In vitro loss and gain of function studies in bladder cancer cell lines.
  • Survival analysis using the Kaplan-Meier method.

Main Results:

  • WNT7B is downregulated in high-grade bladder urothelial carcinomas and associated with poor prognosis.
  • WNT7B inhibits EMT, stem-like properties, and chemoresistance in bladder cancer cells.
  • The WNT7B/FZD5-ELF3-NOTCH1 pathway was identified, with ELF3 modulating the tumor suppressor NOTCH1.

Conclusions:

  • WNT7B/FZD5-ELF3-NOTCH1 signaling acts as a tumor-suppressing pathway in bladder urothelial carcinoma.
  • This pathway represents a potential therapeutic target for improving patient outcomes.
Keywords:
ChemoresistanceEpithelial-mesenchymal transitionWNT7B

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