Figure 3

Selective killing and invasion inhibition of K-ras –transformed cells by capsaicin. A, parental and K-ras–transformed E6E7 cells were incubated with or without 10 μmol/L capsaicin for 4 days in chamber slides. The cells were then stained with hematoxylin and eosin, which show the selective cytotoxicity of capsaicin to K-ras–transformed pancreatic cancer cells (magnification, ×100 and × 400). B, inhibition of cell proliferation by capsaicin in parental and K-ras–transformed E6E7 cells. Cell growth inhibition was measured by long-term MTT assay (mean ± SD of 3 experiments; *P < 0.05). C, measurement of ATP generation after treatment of 1 μmol/L diphenyleneiodonium (DPI) in parental and K-ras –transformed E6E7 cells at various time points as indicated (mean ± SD of 3 experiments). D, measurement results of ATP generation after treatment of 100 nmol/L DPI in normal fibroblasts and naturally occurring pancreatic cancer cells at various time points as indicated (mean ± SD of 3 experiments). E, parental and K-ras–transformed E6E7 cells were seeded onto the chamber insert with a layer of Matrigel matrix, with or without 10 μmol/L capsaicin. Then, 24 hour later, the cells that had digested the Matrigel and migrated to the lower surface of the insert were stained and photographed (magnification, ×100). F, the invasion of K-ras–transformed cells was assessed by counting the number of cells that had migrated onto the lower surface of the insert. The results are presented as the mean ± SD of the numbers from 3 microscopic fields (magnification, ×100). **, P < 0.01.