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. Author manuscript; available in PMC: 2015 Jun 9.
Published in final edited form as: J Natl Cancer Inst. 2006 Dec 20;98(24):1806–1818. doi: 10.1093/jnci/djj498

Fig. 3.

Fig. 3

Effect of cromolyn on S100P-stimulated NFκB promoter activity in pancreatic cancer cells in vitro and in vivo. Panc-1 and BxPC-3 pancreatic cancer cell lines stably expressing an NFκB luciferase reporter were examined for the effects of S100P and cromolyn. A) Panc-1 cells were plated at 5.0 × 103 cells per well, treated for 5 hours with 0, 1, 10, and 100 nM of S100P, with or without cromolyn (100 µ M), and activity of a luciferase gene driven by the NFκB promoter was analyzed. Means and 95% confidence intervals are shown for three independent experiments performed in triplicate. *P = .022, † P <.001, ‡ P <.001 versus control; # P = .005 versus 100 nM S100P alone. B) BxPC-3 cells were plated at 5.0 × 103 cells per well and treated for 5 hours with 0, 1, 10, and 100 µ M of cromolyn, and NFκB reporter luciferase activity was analyzed. Means and 95% confidence intervals are shown for three independent experiments performed in triplicate. *P = .003, † P <.001 versus control. C) BxPC-3 cells stably expressing the NFκB reporter construct were transplanted orthotopically into the pancreas of nude mice. After 1 week, tumor growth was assessed and NFκB activity was analyzed using an IVIS system (Xenogen Corp) after injecting mice with d -luciferin (150 mg/kg body weight) (0 time point). The mice were treated with cromolyn (5 mg/kg body weight by intraperitoneal injection), and NFκB luciferase activity was analyzed again at 24 and 48 hours. *P = .005 versus control. Means and 95% confidence intervals are shown for two independent experiments (n = 4 mice per group). Two-tailed two-sample (unpaired for in vitro and paired for in vivo studies) Student’s t tests were used to determine P values.