Plant phenolics decrease intestinal tumors in an animal model of familial adenomatous polyposis

N N Mahmoud1, A M Carothers, D Grunberger

  • 1The New York Hospital-Cornell Medical Center, 525 East 68th Street, New York, NY 10021, USA.

Carcinogenesis
|April 28, 2000
PubMed

Insights

Plant-derived compounds caffeic acid phenethyl ester (CAPE) and curcumin show promise in preventing colon cancer by reducing tumor formation in mice. These natural compounds may inhibit key stages of carcinogenesis.

Area of Science:

  • Oncology
  • Nutritional Science
  • Molecular Biology

Background:

  • Epidemiological studies link fruit and vegetable consumption to reduced human cancer risk.
  • Plant-derived phenolic compounds exhibit beneficial effects and may inhibit carcinogenesis.
  • Intestinal adenomas can be studied in C57BL/6J-Min/+ mice with an Apc gene mutation.

Purpose of the Study:

  • To investigate the efficacy of plant-derived phenolics (CAPE, curcumin, quercetin, rutin) in preventing intestinal tumors.
  • To assess the impact of these compounds on Apc-associated intestinal carcinogenesis in vivo.
  • To explore the molecular mechanisms underlying tumor prevention by these phenolics.

Main Methods:

  • Administration of CAPE, curcumin, quercetin, and rutin to Min/+ mice at specific dietary levels.
  • Quantification of intestinal tumor formation in treated and control Min/+ mice.
  • Analysis of intestinal tissue for enterocyte apoptosis, proliferation, and beta-catenin expression.

Main Results:

  • CAPE (0.15% diet) reduced tumor formation by 63%; curcumin showed similar inhibition.
  • Quercetin and rutin (2% diet) did not significantly alter tumor formation.
  • Tumor prevention by CAPE and curcumin correlated with increased enterocyte apoptosis and proliferation.
  • CAPE and curcumin decreased oncoprotein beta-catenin expression in enterocytes.

Conclusions:

  • CAPE and curcumin are effective in suppressing Apc-associated intestinal carcinogenesis in mice.
  • These plant phenolics demonstrate potential as chemopreventive agents against colon cancer.
  • The antitumor effects are linked to modulation of apoptosis, proliferation, and beta-catenin signaling.