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Updated: Aug 17, 2025
A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Emerging Developments in ETS-Positive Prostate Cancer Therapy
Gartrell C Bowling1,2, Mitchell G Rands1, Albert Dobi2,3
1School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland.
Abstract:
Prostate cancer is a global health concern, which has a low survival rate in its advanced stages. Even though second-generation androgen receptor-axis inhibitors serve as the mainstay treatment options, utmost of the metastatic cases progress into castration-resistant prostate cancer after their initial treatment response with poor prognostic outcomes. Hence, there is a dire need to develop effective inhibitors that aim the causal oncogenes tangled in the prostate cancer initiation and progression. Molecular-targeted therapy against E-26 transformation-specific (ETS) transcription factors, particularly ETS-related gene, has gained wide attention as a potential treatment strategy. ETS rearrangements with the male hormone responsive transmembrane protease serine 2 promoter defines a significant number of prostate cancer cases and is responsible for cancer initiation and progression. Notably, inhibition of ETS activity has shown to reduce tumorigenesis, thus highlighting its potential as a clinical therapeutic target. In this review, we recapitulate the various targeted drug approaches, including small molecules, peptidomimetics, nucleic acids, and many others, aimed to suppress ETS activity. Several inhibitors have demonstrated ERG antagonist activity in prostate cancer, but further investigations into their molecular mechanisms and impacts on nontumor ETS-containing tissues is warranted.
Insights
Targeting E-26 transformation-specific (ETS) transcription factors offers a promising strategy for advanced prostate cancer. Inhibiting ETS activity, particularly ETS-related gene (ERG), shows potential in reducing tumor growth and improving outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer, especially in advanced stages, presents a significant global health challenge with poor survival rates.
- Current treatments like androgen receptor-axis inhibitors often lead to castration-resistant prostate cancer, necessitating novel therapeutic strategies.
- ETS gene rearrangements are key drivers in a substantial number of prostate cancer cases, influencing initiation and progression.
Approach:
- This review explores molecular-targeted therapies aimed at suppressing E-26 transformation-specific (ETS) transcription factor activity.
- Various drug modalities, including small molecules, peptidomimetics, and nucleic acids, are discussed for their potential to inhibit ETS.
- The focus is on targeting ETS-related gene (ERG) as a critical oncogene in prostate cancer.
Key Points:
- Inhibition of ETS activity has demonstrated a reduction in tumorigenesis, establishing it as a viable clinical therapeutic target.
- Several compounds exhibit ERG antagonist activity, showing promise in preclinical or early clinical settings.
- Understanding the precise molecular mechanisms and off-target effects on non-tumor tissues is crucial for further development.
Conclusions:
- Targeted inhibition of ETS transcription factors represents a rational approach to combatting castration-resistant prostate cancer.
- Developing effective ETS inhibitors could overcome limitations of current therapies and improve patient prognosis.
- Further research is essential to refine these targeted therapies and ensure their safety and efficacy.
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