BACKGROUND: Colorectal cancer (CRC) is one of the most common and preventable cancers. Regular consumption of apples is conducive to reduction in CRC risk. AIM OF THE STUDY: To evaluate effects of modified apple polysaccharide (MAP) on tumorigenesis in a mouse model of colitis-associated colon cancer. METHODS: One hundred male ICR mice were administered with 1, 2-dimethyl-hydrazine (DMH) and dextran sodium sulfate (DSS). Forty mice were given no further treatment, the rest were fed basal diet blended with three different doses of MAP; 2.5, 5, and 10% (20 mice in each group). RESULTS: MAP significantly protected ICR mice against DMH/DSS-induced tumorigenesis. The incidence of tumor development was 90% (18/20) in the mice treated with DMH/DSS, but that was reduced to 25% (5/20), 15% (3/20), and 5% (1/20), respectively, in the mice treated with basal diets plus 2.5, 5, and 10% of MAP. Study of apoptosis of colonic epithelial cells revealed that MAP moderately increased apoptosis, suggesting that the anti-tumor potency of MAP was probably attributed to its ability to induce apoptosis. Western blot analysis demonstrated that carbohydrate-binding protein galectin-3 changed in both the nucleus and the cytoplasm during the process from colitis to colon cancer in the model. And MAP could inhibit the binding of galectin-3 to its ligand: this is, at least in part, the possible mechanism of MAP by enhancing apoptosis and preventing tumorigenesis. CONCLUSIONS: These data suggest that MAP has a potential role in clinical prevention and treatment for colon cancer.
BACKGROUND:Colorectal cancer (CRC) is one of the most common and preventable cancers. Regular consumption of apples is conducive to reduction in CRC risk. AIM OF THE STUDY: To evaluate effects of modified apple polysaccharide (MAP) on tumorigenesis in a mouse model of colitis-associated colon cancer. METHODS: One hundred male ICR mice were administered with 1, 2-dimethyl-hydrazine (DMH) and dextran sodium sulfate (DSS). Forty mice were given no further treatment, the rest were fed basal diet blended with three different doses of MAP; 2.5, 5, and 10% (20 mice in each group). RESULTS: MAP significantly protected ICR mice against DMH/DSS-induced tumorigenesis. The incidence of tumor development was 90% (18/20) in the mice treated with DMH/DSS, but that was reduced to 25% (5/20), 15% (3/20), and 5% (1/20), respectively, in the mice treated with basal diets plus 2.5, 5, and 10% of MAP. Study of apoptosis of colonic epithelial cells revealed that MAP moderately increased apoptosis, suggesting that the anti-tumor potency of MAP was probably attributed to its ability to induce apoptosis. Western blot analysis demonstrated that carbohydrate-binding protein galectin-3 changed in both the nucleus and the cytoplasm during the process from colitis to colon cancer in the model. And MAP could inhibit the binding of galectin-3 to its ligand: this is, at least in part, the possible mechanism of MAP by enhancing apoptosis and preventing tumorigenesis. CONCLUSIONS: These data suggest that MAP has a potential role in clinical prevention and treatment for colon cancer.
Authors: Gabriel A Rabinovich; Linda G Baum; Nicola Tinari; Roberto Paganelli; Clara Natoli; Fu Tong Liu; Stefano Iacobelli Journal: Trends Immunol Date: 2002-06 Impact factor: 16.687
Authors: Pratima Nangia-Makker; Victor Hogan; Yuichiro Honjo; Sara Baccarini; Larry Tait; Robert Bresalier; Avraham Raz Journal: J Natl Cancer Inst Date: 2002-12-18 Impact factor: 13.506
Authors: Axel S Merseburger; Mario W Kramer; Jörg Hennenlotter; Perikles Simon; Judith Knapp; Jörg T Hartmann; Arnulf Stenzl; Jürgen Serth; Markus A Kuczyk Journal: Prostate Date: 2008-01-01 Impact factor: 4.104