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SULT2B1b sulfotransferase: induction by vitamin D receptor and reduced expression in prostate cancer

Young-Kyo Seo1, Nooshin Mirkheshti, Chung S Song

  • 1Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78245, USA.

Molecular Endocrinology (Baltimore, Md.)
|April 13, 2013
PubMed

Insights

Reduced sulfotransferase 2B1b (SULT2B) in prostate tumors may fuel cancer growth by increasing active androgens. Restoring SULT2B levels could potentially inhibit prostate cancer progression.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Recurrent prostate cancer reactivates androgen receptors, driven by intratumor 5α-dihydrotestosterone synthesis from dehydroepiandrosterone (DHEA).
  • Key enzymes like 3β-hydroxysteroid dehydrogenase (3β-HSD1), aldoketoreductase (AKR1C3), and steroid 5-alpha reductase, type 1 (SRD5A1) fuel this process.
  • Sulfotransferase 2B1b (SULT2B) converts DHEA to inactive sulfates, potentially limiting androgen synthesis.

Purpose of the Study:

  • To investigate the role of SULT2B expression in treatment-naive prostate cancer tissue.
  • To explore the regulation of SULT2B by vitamin D receptor (VDR).
  • To assess the impact of SULT2B levels on prostate cancer cell proliferation.

Main Methods:

  • Immunohistochemistry and immunoblotting were used to analyze SULT2B expression in prostatectomy specimens.
  • The SULT2B1 promoter activity was studied in vitro and in vivo using VDR activation.
  • Prostate cancer cell proliferation was assessed after SULT2B knockdown and DHEA stimulation.

Main Results:

  • SULT2B expression was significantly reduced in malignant prostate tissue compared to adjacent nonmalignant glands.
  • Vitamin D receptor activation induced SULT2B expression in mouse prostate and prostate cancer cells.
  • SULT2B knockdown accelerated prostate cancer cell proliferation when stimulated by DHEA.

Conclusions:

  • Tumor tissue SULT2B levels may influence prostate cancer growth.
  • Reduced SULT2B in tumors may contribute to increased androgen synthesis and cancer progression.
  • Therapeutic induction of SULT2B could be a potential strategy to inhibit prostate cancer progression.

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