Peanut lectin stimulates proliferation in colonic explants from patients with inflammatory bowel disease and colon polyps.

BACKGROUND/AIMS: The TF antigen (galactose-beta 1,3-N-acetylgalactosamine alpha) is overexpressed in malignant and premalignant colonic epithelium. Previous studies have shown that peanut lectin (PNA), which binds TF, is mitogenic for normal human colonic epithelium. This study aimed to determine its effect on abnormal colonic epithelium.
METHODS: Crypt cell proliferation rate (CCPR) was measured using vincristine arrest and mucus synthesis by incorporation of radiolabeled N-acetyl glucosamine in colonoscopic biopsy specimens cultured with and without PNA.
RESULTS: Unstimulated CCPR was greater in patients with ulcerative colitis than in patients with histologically normal colon. PNA (25 micrograms/mL) produced a 25% average increase in CCPR in tissues from patients with ulcerative colitis, Crohn's disease, and colonic polyps. In ulcerative colitic biopsy specimens incubated with PNA, CCPR increased to more than double that of unstimulated normal colonic epithelium. In controls, the response to PNA was greater when adjacent specimens were positive for PNA (avidin-biotin) histochemistry than when they were negative. Mucus synthesis was increased by an average 75% over 24 hours by PNA.
CONCLUSIONS: Increased TF expression by premalignant epithelia may allow stimulation of proliferation by dietary galactose N-acetylgalactosamine-binding lectins. If the hyperplasia-dysplasia cancer hypothesis is correct, this could explain the increased colon cancer risk in ulcerative colitis.