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The transcription factor SNAIL represses vitamin D receptor expression and responsiveness in human colon cancer

Héctor G Pálmer1, María Jesús Larriba, José Miguel García

  • 1Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, E-28029 Madrid, Spain.

Nature Medicine
|August 24, 2004
PubMed

Insights

The SNAIL transcription factor reduces vitamin D receptor (VDR) expression in colon cancer, hindering the effectiveness of vitamin D therapies. This finding reveals a new mechanism impacting cancer treatment outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Non-hypercalcemic analogs of 1alpha,25-dihydroxyvitamin D3 (1,25(OH)(2)D(3)) exhibit antitumor properties in some cancer patients.
  • High vitamin D receptor (VDR) expression is linked to a favorable prognosis but diminishes during tumor progression.

Purpose of the Study:

  • To investigate the role of the SNAIL transcription factor in regulating VDR gene expression in human colon cancer cells.
  • To determine if SNAIL influences the efficacy of 1,25(OH)(2)D(3) analogs in preclinical models.

Main Methods:

  • Utilized human colon cancer cell lines to study VDR gene expression.
  • Employed xenograft mouse models to assess the antitumor activity of a 1,25(OH)(2)D(3) analog (EB1089).
  • Correlated SNAIL and VDR expression levels in human colon cancer tissues.

Main Results:

  • The SNAIL transcription factor was found to repress VDR gene expression in human colon cancer cells.
  • SNAIL expression inhibited the antitumor effects of EB1089 in a mouse xenograft model.
  • Elevated SNAIL expression in human colon cancers correlated with reduced VDR expression.

Conclusions:

  • SNAIL acts as a repressor of VDR expression in colon cancer.
  • Targeting SNAIL may restore VDR expression and enhance the efficacy of vitamin D-based therapies for colon cancer.

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