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Updated: Feb 5, 2026

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
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Isolation of Cancer Stem Cells From Human Prostate Cancer Samples

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Functional Silencing of HSD17B2 in Prostate Cancer Promotes Disease Progression

Xiaomei Gao1,2, Charles Dai3, Shengsong Huang4

  • 1State Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, P.R. China.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|September 20, 2018
PubMed
Abstract

Insights

Enzyme HSD17B2 inactivates androgens, crucial for prostate cancer. Its silencing via DNA methylation and alternative splicing promotes tumor growth, offering new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Steroidogenic enzymes are critical for prostate cancer progression.
  • Enzymes that inactivate potent androgens are understudied, limiting therapeutic options.
  • Understanding androgen-inactivating enzymes is key to developing novel prostate cancer treatments.

Purpose of the Study:

  • To investigate the clinical relevance, significance, and regulatory mechanisms of HSD17B2 in prostate cancer.
  • To explore HSD17B2's role in androgen metabolism and signaling pathways.
  • To identify potential therapeutic strategies targeting HSD17B2 functional silencing.

Main Methods:

  • Detected HSD17B2 expression in patient specimens and cell lines.
  • Assessed HSD17B2 function in steroidogenesis, androgen receptor signaling, and tumor growth using cell lines and xenografts.
  • Investigated DNA methylation and mRNA alternative splicing as regulatory mechanisms.

Main Results:

  • HSD17B2 expression decreases with prostate cancer progression.
  • Overexpression of HSD17B2 suppressed androgen-induced proliferation and xenograft growth.
  • Functional silencing of HSD17B2 involves DNA methylation and alternative splicing, generating degradation-promoting isoforms.

Conclusions:

  • HSD17B2 plays a significant role in prostate cancer progression.
  • Functional silencing mechanisms of HSD17B2, including DNA methylation and alternative splicing, are clinically relevant.
  • Targeting HSD17B2 silencing offers potential new strategies for prostate cancer management.

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