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Classical and Non-Classical Roles for Pre-Receptor Control of DHT Metabolism in Prostate Cancer Progression

Ailin Zhang1, Jiawei Zhang2, Stephen Plymate3

  • 1Division of Clinical Research, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, MS D5-380, Seattle, WA, 98109, USA.

Hormones & Cancer
|January 23, 2016
PubMed

Insights

Enzymes controlling androgen metabolism influence prostate cancer (PCa) progression. Targeting these enzymes may offer new strategies against castration-resistant PCa (CRPC) by managing intratumoral androgens.

Area of Science:

  • Oncology
  • Endocrinology
  • Biochemistry

Background:

  • Androgens are crucial in prostate cancer (PCa) development and progression.
  • Androgen deprivation therapy (ADT) is a front-line treatment, but resistance leads to castration-resistant PCa (CRPC).
  • Tumor microenvironments in CRPC retain androgens capable of activating the androgen receptor (AR).

Purpose of the Study:

  • To review emerging data on enzymes controlling pre-receptor metabolism of dihydrotestosterone (DHT).
  • To explore the role of these enzymes in regulating intratumoral androgens and influencing PCa progression.
  • To discuss the potential unrecognized role of these enzymes in CRPC progression.

Main Methods:

  • Review of expression data for steroidogenic enzymes in primary PCa and CRPC.
  • Analysis of enzyme activity and regulation in experimental PCa models.
  • Examination of the impact of genetic variations in DHT metabolism genes on PCa risk.

Main Results:

  • Specific enzymes (AKR1C2, HSD17B6, HSD17B10, UGT2B15, UGT2B17) are implicated in controlling intratumoral androgens.
  • Expression and activity of these enzymes vary in PCa and CRPC.
  • Genetic variations in these genes may affect PCa risk.

Conclusions:

  • Enzymes mediating pre-receptor DHT metabolism are key regulators of intratumoral androgens in PCa.
  • These enzymes influence PCa progression and may play a role in CRPC development.
  • Further research into these enzymes could reveal novel therapeutic targets for CRPC.

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