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An Orthotopic Murine Model of Human Prostate Cancer Metastasis
06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

Dietary folate deficiency blocks prostate cancer progression in the TRAMP model

Gaia Bistulfi1, Barbara A Foster, Ellen Karasik

  • 1Department of Cancer Genetics, Roswell Park Cancer Institute, Elm & Carlton streets, BLSC L3-314, Buffalo, NY 14263, USA.

Cancer Prevention Research (Philadelphia, Pa.)
|August 13, 2011
PubMed

Insights

Mild dietary folate depletion significantly arrested prostate cancer progression in mice. This suggests that targeting folate metabolism could be a promising strategy for treating prostate cancer.

Area of Science:

  • Oncology
  • Nutritional Science
  • Molecular Biology

Background:

  • Dietary folate is crucial for cellular functions, including proliferation and maintaining metabolic pools.
  • Prostate cells exhibit a higher demand for folate due to their metabolic activity, impacting proliferation and genomic stability.
  • The effect of dietary folate on prostate cancer progression remains largely unexplored, unlike its known impact on colon cancer models.

Purpose of the Study:

  • To investigate the impact of dietary folate manipulation on prostate cancer progression.
  • To determine if prostate epithelial cell metabolism is significantly influenced by folate levels in the context of cancer.

Main Methods:

  • Utilized the transgenic adenoma of the mouse prostate (TRAMP) model for prostate-specific tumorigenesis.
  • Administered mild dietary folate depletion and supplementation to TRAMP mice.
  • Analyzed tumor size, grade, proliferation, and apoptosis to assess cancer progression.
  • Characterized folate and metabolite pools, genetic/epigenetic damage, and enzyme expression in prostate tissue.

Main Results:

  • Mild dietary folate depletion led to the arrest of prostate cancer progression in 25 out of 26 TRAMP mice.
  • Folate depletion significantly impacted tumor size, grade, proliferation, and apoptosis.
  • Folate supplementation showed a mild, non-significant positive effect on tumor grade.
  • Observed correlations between folate/metabolite pools, genetic/epigenetic damage, enzyme expression, and tumor progression.

Conclusions:

  • Prostate cancer demonstrates high sensitivity to dietary folate levels.
  • Antifolate therapies, in conjunction with existing treatments, may offer improved therapeutic outcomes for prostate cancer.
  • Dietary folate manipulation presents a potential novel strategy for managing prostate cancer.

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