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Alterations In Tumor Aggression Following Androgen Receptor Signaling Restoration In Canine Prostate Cancer Cell Lines.

Home
Research Domains
Biomedical And Clinical Sciences
Oncology And Carcinogenesis
Predictive And Prognostic Markers
Alterations In Tumor Aggression Following Androgen Receptor Signaling Restoration In Canine Prostate Cancer Cell Lines.

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Alterations in Tumor Aggression Following Androgen Receptor Signaling Restoration in Canine Prostate Cancer Cell Lines.

Demitria M Vasilatis^1,2, Neelu Batra^2,3, Christopher A Lucchesi^1,2

¹Department of Urologic Surgery, School of Medicine, University of California Davis, Sacramento, CA 95718, USA.

International Journal of Molecular Sciences

|August 29, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Restoring androgen receptor (AR) in canine prostate cancer (PCa) models showed varied effects. While one model exhibited tumor suppression, others displayed altered proliferation, migration, and invasion, highlighting PCa heterogeneity.

Keywords:

androgen indifferent prostate cancer androgen receptor dog prostate cancer

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Area of Science:

Oncology
Molecular Biology
Comparative Pathology

Background:

Androgen receptor (AR) signaling plays a dual role in prostate cancer (PCa), promoting tumorigenesis in cancerous tissue but suppressing aggressive behaviors in benign tissue.
Canine PCa is a natural model for human PCa, yet canine PCa often lacks AR expression, limiting its utility in studying AR's therapeutic potential.
Understanding AR's function in PCa is crucial for developing effective therapeutic strategies.

Purpose of the Study:

To investigate the effects of restoring AR signaling in AR-null canine PCa cell lines.
To characterize the resultant changes in tumorigenic behaviors, including clonogenicity, viability, migration, and invasion.
To explore the role of AR in regulating tumor suppressor genes and epithelial-mesenchymal transition (EMT) markers.

Main Methods:

Three AR-null canine PCa cell lines (1508, Leo, 1258) were transfected with canine wild-type AR.
Cells were treated with dihydrotestosterone (DHT) to activate the restored AR.
Assays were performed to measure clonogenicity, viability, migration, and invasion. Gene expression of NKX3.1, FOLH1, Vimentin, N-cadherin, and SNAIL1 was analyzed. siRNA-mediated knockdown of Vimentin was used to assess its role in AR-induced migration.

Main Results:

In the 1508 cell line, AR restoration significantly decreased clonogenicity, viability, migration, and invasion, while increasing the tumor suppressor NKX3.1 expression.
In the Leo cell line, AR decreased clonogenicity and altered FOLH1 and NKX3.1 expression. EMT markers increased, but AR did not affect migration or invasion.
In the 1258 cell line, AR increased migration and invasion, accompanied by increased EMT marker expression. AR did not affect proliferation in this line.

Conclusions:

AR restoration has heterogeneous effects on canine PCa cell lines, demonstrating cell line-specific responses.
The 1508 cell line exhibited AR-mediated tumor suppression, while Leo showed effects on proliferation and 1258 showed AR- and EMT-driven migration and invasion.
These findings underscore the complexity of AR signaling in PCa and highlight the importance of considering cell line-specific characteristics in canine models.