BACKGROUND: Inositol hexaphosphate (IP6) is a naturally occurring polyphosphorylated carbohydrate found in food sources high in fiber content. IP6 has been reported to have significant inhibitory effects against a variety of primary tumors including breast and colon. The effects of IP6 have not been evaluated in pancreatic cancer. We hypothesized that IP6 would significantly inhibit cell growth and increase the apoptotic rate of pancreatic cancer in vitro. MATERIALS AND METHODS: Two pancreatic cancer cell lines (MIAPACA and PANC1) were cultured using standard techniques and treated with IP6 at doses of 0.5, 1.0, and 5.0 mm. Cell viability was measured by MTT at 24 and 72 h. Apoptosis was evaluated by Annexin V-FITC and results calculated using FACS analysis. Statistical analysis was performed by ANOVA. RESULTS: Significant reductions (P < 0.01) in cellular proliferation were observed with all IP6 concentrations tested in both cell lines and at both time points. Reductions in cell proliferation ranged from 37.1 to 91.5%. IP6 increased early and late apoptotic activity (P < 0.01). CONCLUSIONS: Treatment of pancreatic cancer with the common dietary polyphosphorylated carbohydrate IP6 significantly decreased cellular growth and increased apoptosis. Our findings suggest that IP6 has the potential to become an effective adjunct for pancreatic cancer treatment. Further in vivo and human studies are needed to evaluate safety and clinical utility of this agent in patients with pancreatic cancer.
BACKGROUND:Inositol hexaphosphate (IP6) is a naturally occurring polyphosphorylated carbohydrate found in food sources high in fiber content. IP6 has been reported to have significant inhibitory effects against a variety of primary tumors including breast and colon. The effects of IP6 have not been evaluated in pancreatic cancer. We hypothesized that IP6 would significantly inhibit cell growth and increase the apoptotic rate of pancreatic cancer in vitro. MATERIALS AND METHODS: Two pancreatic cancer cell lines (MIAPACA and PANC1) were cultured using standard techniques and treated with IP6 at doses of 0.5, 1.0, and 5.0 mm. Cell viability was measured by MTT at 24 and 72 h. Apoptosis was evaluated by Annexin V-FITC and results calculated using FACS analysis. Statistical analysis was performed by ANOVA. RESULTS: Significant reductions (P < 0.01) in cellular proliferation were observed with all IP6 concentrations tested in both cell lines and at both time points. Reductions in cell proliferation ranged from 37.1 to 91.5%. IP6 increased early and late apoptotic activity (P < 0.01). CONCLUSIONS: Treatment of pancreatic cancer with the common dietary polyphosphorylated carbohydrateIP6 significantly decreased cellular growth and increased apoptosis. Our findings suggest that IP6 has the potential to become an effective adjunct for pancreatic cancer treatment. Further in vivo and human studies are needed to evaluate safety and clinical utility of this agent in patients with pancreatic cancer.