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Updated: Mar 6, 2026
A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Development of 17β-hydroxysteroid dehydrogenase type 3 as a target in hormone-dependent prostate cancer therapy
Xiaohui Ning1, Yan Yang2, Hong Deng1
1Institute of Materia Medica and Guangdong Provincial Key Laboratory of New Pharmaceutical Dosage Form, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, PR China.
Abstract:
17β-Hydroxysteroid dehydrogenase type 3 (17β-HSD3) is expressed almost exclusively in the testes and specifically converts the weak androgenic androstenedione to active testosterone (T) in the presence of NADPH. Additionally, studies have demonstrated that 17β-HSD3 is over-expressed in hormone-dependent prostate cancer. T, which interacts with the androgen receptor (AR), eventually stimulates the growth of prostate cancer cells. Defects in T synthesis or action impair the development of the male phenotype during embryogenesis and cause the autosomal recessive disorder male pseudohermaphroditism. Affected individuals are often born with female-appearing external genitalia and are reared as females. Since 17β-HSD3 plays a central role in T production, it has been recognized as a promising therapeutic target to reduce the circulating level of androgens and to suppress androgen-sensitive tumor proliferation. In recent decades, improvements have been made in the development of 17β-HSD3 inhibitors. Herein, we give an overview of the main structure and function of human 17β-HSD3 and summarize steroidal and non-steroidal inhibitors of 17β-HSD3, which can be a potential target for prostate cancer.
Insights
17β-Hydroxysteroid dehydrogenase type 3 (17β-HSD3) is crucial for testosterone production and is over-expressed in prostate cancer. Inhibitors targeting 17β-HSD3 offer a promising therapeutic strategy for treating hormone-dependent prostate cancer.
Area of Science:
- Biochemistry
- Endocrinology
- Oncology
Background:
- 17β-Hydroxysteroid dehydrogenase type 3 (17β-HSD3) catalyzes the conversion of androstenedione to testosterone (T), the active androgen.
- Over-expression of 17β-HSD3 in prostate cancer promotes tumor growth by increasing T levels.
- Defects in 17β-HSD3 cause male pseudohermaphroditism, highlighting its critical role in male development.
Purpose of the Study:
- To provide an overview of the structure and function of human 17β-HSD3.
- To summarize existing steroidal and non-steroidal inhibitors of 17β-HSD3.
- To highlight 17β-HSD3 as a therapeutic target for prostate cancer.
Main Methods:
- Literature review of 17β-HSD3 structure, function, and inhibitors.
- Analysis of the role of 17β-HSD3 in testosterone synthesis and prostate cancer progression.
Main Results:
- 17β-HSD3 is a key enzyme in androgen biosynthesis, primarily active in the testes.
- 17β-HSD3 inhibitors have been developed, showing potential for therapeutic applications.
- Targeting 17β-HSD3 can reduce androgen levels and suppress prostate cancer proliferation.
Conclusions:
- 17β-HSD3 is a validated therapeutic target for hormone-dependent prostate cancer.
- Development of 17β-HSD3 inhibitors represents a promising strategy for prostate cancer treatment.
- Further research into 17β-HSD3 inhibitors could lead to novel therapies for androgen-sensitive cancers.
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