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17β-Hydroxysteroid Dehydrogenase Type 2 Expression Is Induced by Androgen Signaling in Endometrial Cancer

Chiaki Hashimoto1, Yasuhiro Miki2, Sota Tanaka3

  • 1Department of Obstetrics and Gynecology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan. chiaki@med.tohoku.ac.jp.

International Journal of Molecular Sciences
|April 13, 2018
PubMed

Insights

Androgen suppresses endometrial cancer growth by increasing 17β-hydroxysteroid dehydrogenase type 2 (17β-HSD2). This enzyme reduces estrogen

Area of Science:

  • Gynecologic Oncology
  • Endocrinology
  • Cancer Biology

Background:

  • Endometrial cancer is a common female pelvic cancer linked to androgens.
  • Androgen's anti-cancer mechanisms in endometrial cancer are not fully understood.
  • 17β-hydroxysteroid dehydrogenase type 2 (17β-HSD2) converts estradiol (E2) to estrone (E1) and is upregulated by androgens in breast cancer.

Purpose of the Study:

  • To investigate the role of androgens in endometrial cancer's estrogen dependence.
  • To explore the function of 17β-HSD2 in androgen-mediated effects on endometrial cancer.

Main Methods:

  • Dihydrotestosterone (DHT) treatment of HEC-1B endometrial cancer cells to assess 17β-HSD2 expression and proliferation.
  • Measurement of intratumoral DHT levels in endometrioid endometrial adenocarcinoma (EEA) tissues.
  • Immunohistochemical analysis of 17β-HSD2, Ki-67, progesterone receptors, and androgen receptors in EEA tissues.
  • Correlation analysis between 17β-HSD2 status and clinicopathological parameters and patient survival.

Main Results:

  • DHT induced 17β-HSD2 mRNA and protein expression in HEC-1B cells.
  • DHT inhibited estradiol-induced proliferation of HEC-1B cells.
  • Intratumoral DHT levels correlated with 17β-HSD2 status in EEA tissues.
  • 17β-HSD2 expression was inversely associated with tumor grade, stage, and Ki-67, and positively correlated with progesterone receptor and androgen receptor status.
  • 17β-HSD2-positive patients showed improved progression-free and cancer-specific survival.

Conclusions:

  • Androgen suppresses endometrial cancer estrogen dependence by inducing 17β-HSD2.
  • 17β-HSD2 may serve as a biomarker for better prognosis in endometrial cancer.
  • Targeting the androgen-estrogen-17β-HSD2 axis could offer therapeutic strategies for endometrial cancer.
Keywords:
17β-hydroxysteroid dehydrogenase type 2androgenendometrial cancerendometrioid endometrial adenocarcinoma

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