CD271 promotes proliferation and migration in bladder cancer.
Shingo Myoen1,2,3, Mai Mochizuki1, Rie Shibuya-Takahashi1
1Division of Cancer Stem Cell, Miyagi Cancer Center Research Institute, Natori, Miyagi, Japan.
Genes to Cells : Devoted to Molecular & Cellular Mechanisms
|November 28, 2023
Summary
CD271, a receptor, drives bladder cancer growth and spread. Inhibiting CD271 reduces tumor formation and improves survival, highlighting its potential as a therapeutic target for advanced urothelial cancer.
Area of Science:
- Oncology
- Cell Biology
- Molecular Medicine
Background:
- Bladder cancer, a urothelial carcinoma, has limited treatment options for advanced stages.
- CD271, a neurotrophin receptor, has an emerging role in cancer progression.
Purpose of the Study:
- To investigate the role of CD271 in bladder cancer proliferation, migration, and tumorigenicity.
- To explore the molecular pathways regulated by CD271 in bladder cancer.
- To correlate CD271 expression with clinical outcomes in bladder cancer patients.
Main Methods:
- CD271 knockdown and overexpression in bladder cancer cell lines.
- In vivo tumorigenicity assays.
- Migration assays using TAT-Pep5 inhibitor.
- Gene expression analysis (E2F, Myc pathways).
- Immunohistochemical analysis of clinical specimens (pERK colocalization).
Main Results:
- CD271 overexpression increased bladder cancer cell proliferation and migration; knockdown decreased these.
- CD271 depletion impaired tumor growth in vivo and induced apoptosis.
- Gene expression analysis revealed CD271 affects E2F and Myc pathways.
- High CD271 expression correlated with significantly shorter overall survival in patients.
- CD271 colocalized with pERK in clinical samples.
Conclusions:
- CD271 promotes bladder cancer cell proliferation and migration, contributing to malignancy.
- CD271 is a potential therapeutic target for advanced bladder cancer.
- CD271 expression is a prognostic marker for poor survival in bladder cancer.
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