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Updated: Oct 27, 2025
Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
Characterization of Novel Progression Factors in Castration-Resistant Prostate Cancer Based on Global Comparative
Ann-Yae Na1, Soyoung Choi1, Eunju Yang2
1BK21 FOUR Community-Based Intelligent Novel Drug Discovery Education Unit, College of Pharmacy, Kyungpook National University, Daegu 41566, Korea.
Abstract:
Identifying the biological change from hormone-naïve prostate cancer to castration-resistant prostate cancer (CRPC) is a major clinical challenge for developing therapeutic agents. Although the pathways that lead to CRPC are not fully completely understood, recent evidence demonstrates that androgen signaling is often maintained through varied mechanisms. Androgen deprivation therapy (ADT) is used as a primary treatment for preventing the progression of prostate cancer (PCa). Here we investigated PCa tissues at each stage of progression, from benign prostatic hyperplasia (BPH) to CRPC, based on quantitative proteomic technology, including tissues after ADT. In total, 4768 proteins were identified in this study, of which 4069 were quantified in the combined PCa tissues. Among the quantified proteins, 865 were differentially expressed proteins (21.2%). Based on the quantitative protein results, we performed systematic bioinformatics analysis and found that the levels of 15 proteins, including FOXA1 and HMGN1-3, increased among T3G3, T3GX, and CRPC, despite the ADT. Among all targets, we verified the increased levels of FOXA1 and HMGN1-3 in CRPC by immunoblotting and indirect enzyme-linked immunosorbent assay. In summary, we discuss the changes in intracellular factors involved in the progression of CRPC PCa despite ADT. Moreover, we suggest that FOXA1 and HMGN1-3 proteins could be used as potential CRPC-related factors in clinical therapeutic agents.
Insights
Identifying key protein changes in prostate cancer (PCa) progression is crucial. This study reveals FOXA1 and HMGN1-3 proteins increase in castration-resistant prostate cancer (CRPC) despite treatment, suggesting potential therapeutic targets.
Area of Science:
- Oncology
- Proteomics
- Molecular Biology
Background:
- Prostate cancer (PCa) progression to castration-resistant prostate cancer (CRPC) presents a significant clinical challenge.
- Androgen deprivation therapy (ADT) is a primary treatment, but resistance mechanisms remain incompletely understood.
- Androgen signaling often persists in CRPC through various pathways.
Purpose of the Study:
- To investigate proteomic changes during prostate cancer progression, from benign prostatic hyperplasia (BPH) to CRPC.
- To identify proteins that change in expression despite Androgen Deprivation Therapy (ADT).
- To explore potential biomarkers for CRPC progression.
Main Methods:
- Quantitative proteomic analysis of PCa tissues across different stages (BPH to CRPC), including post-ADT samples.
- Bioinformatics analysis of identified and quantified proteins.
- Validation of key protein level changes using immunoblotting and ELISA.
Main Results:
- 4768 proteins identified, 4069 quantified in PCa tissues.
- 865 differentially expressed proteins (21.2%) were found.
- Levels of 15 proteins, including FOXA1 and HMGN1-3, increased in advanced stages (T3G3, T3GX, CRPC) despite ADT.
Conclusions:
- Intracellular factors, such as FOXA1 and HMGN1-3, play a role in CRPC progression even with ADT.
- Increased FOXA1 and HMGN1-3 levels are observed in CRPC.
- FOXA1 and HMGN1-3 are potential therapeutic targets and biomarkers for CRPC.
