BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells. In this study, we investigated the sensitization effects of scutellarin (SC), a compound isolated from the traditional Chinese herb Erigeron breviscapus, on RSV and 5-FU-evoked apoptosis of these cancer cells. MATERIALS AND METHODS: The drug-induced apoptosis was qualified by TUNEL staining under fluorescence microscopy, before being quantified by propiodium iodide staining through flow cytometric assay. RESULTS: SC (100 microM) sensitized RSV- (200 microM) and 5-FU (500 microM)-evoked apoptosis in p53+/+ but not p53(-/-) cells. RSV- and 5-FU-elicited caspase-6 activation was promoted by SC in a time-dependent manner. SC itself did not trigger apoptosis or caspase-6 activation at the concentration tested. CONCLUSION: SC is a novel sensitizing agent for both RSV- and 5-FU-evoked apoptosis, through the enhancement of caspase-6 activation in a p53-dependent manner.
BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 humancolon cancer cells. In this study, we investigated the sensitization effects of scutellarin (SC), a compound isolated from the traditional Chinese herb Erigeron breviscapus, on RSV and 5-FU-evoked apoptosis of these cancer cells. MATERIALS AND METHODS: The drug-induced apoptosis was qualified by TUNEL staining under fluorescence microscopy, before being quantified by propiodium iodide staining through flow cytometric assay. RESULTS: SC (100 microM) sensitized RSV- (200 microM) and 5-FU (500 microM)-evoked apoptosis in p53+/+ but not p53(-/-) cells. RSV- and 5-FU-elicited caspase-6 activation was promoted by SC in a time-dependent manner. SC itself did not trigger apoptosis or caspase-6 activation at the concentration tested. CONCLUSION: SC is a novel sensitizing agent for both RSV- and 5-FU-evoked apoptosis, through the enhancement of caspase-6 activation in a p53-dependent manner.