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CCAAT/enhancer-binding protein delta: a molecular target of 1,25-dihydroxyvitamin D3 in androgen-responsive prostate

Takayuki Ikezoe1, Sigal Gery, Dong Yin

  • 1Division of Hematology/Oncology, Cedars-Sinai Medical Center, University of California at Los Angeles School of Medicine, Los Angeles, California, USA. ikezoet@med.kochi-ms.ac.jp

Cancer Research
|June 3, 2005
PubMed

Insights

The active vitamin D3 metabolite, 1,25(OH)2D3, inhibits prostate cancer growth by up-regulating CCAAT/enhancer-binding protein delta (C/EBPdelta). This protein is crucial for vitamin D3

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • 1,25-Dihydroxyvitamin D3 [1,25(OH)2D3], the active form of vitamin D3, is known to inhibit prostate cancer cell proliferation.
  • The precise molecular mechanisms underlying this inhibitory effect are not fully understood.

Purpose of the Study:

  • To identify target genes of 1,25(OH)2D3 in prostate cancer cells using microarray analysis.
  • To elucidate the role of CCAAT/enhancer-binding protein delta (C/EBPdelta) in the anti-proliferative effects of 1,25(OH)2D3.

Main Methods:

  • Microarray technology was employed to identify genes modulated by 1,25(OH)2D3 in LNCaP prostate cancer cells.
  • RNA interference was used to knock down C/EBPdelta expression.
  • Forced expression of C/EBPdelta was performed in various cancer cell lines.

Main Results:

  • 1,25(OH)2D3 significantly up-regulated C/EBPdelta by approximately 5-fold in LNCaP cells.
  • Knockdown of C/EBPdelta abrogated the growth inhibitory effects of 1,25(OH)2D3 on LNCaP cells.
  • 1,25(OH)2D3 induced C/EBPdelta in hormone-sensitive breast cancer cells (MCF-7, T47D) but not in hormone-insensitive cells (PC-3, DU145, MDA-MB-231).
  • Forced expression of C/EBPdelta markedly reduced clonal growth in prostate and breast cancer cells.

Conclusions:

  • C/EBPdelta is a key mediator of 1,25(OH)2D3-induced growth inhibition in prostate and breast cancer cells.
  • The induction of C/EBPdelta by 1,25(OH)2D3 is dependent on the presence of specific hormone receptors (androgen or estrogen receptors).
  • Therapeutic strategies involving the forced expression of C/EBPdelta show promise for cancer treatment.

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