| Objective To observe the effect of casticin(CAS) on the growth and apoptosis of human colon cancer SW480 cells, and explore whether the mechanism underlying CAS induces apoptosis is involved in up-regulate the expression of death receptors-5 (DR5) and inhibition of nuclear factor kappaB (NF-κB) activity.Methods Human colon cancer SW480 cells cultured in vitro.The capability of anchoring dependent growth in SW480 cells was determined using agar colony formation assay. Fluorescence microscopy with Hoechst 33258 fluorescence staining was used to observe morphology of apoptotic cells.flow cytometry(FCM) analysis after PI staining and (FCM) was used to examine apoptosis rate in SW480 cells.Western Blotting was used to analyze the expression of DR5 and NF-κB (p65) protein.Result Agar colony formation assay showed that CAS inhibited growth of SW480, in a dose-dependent( 0.05). The apoptotic morphous such as nuclear chromatin condensation was observed by fluorescence microscopy after Hoechst 33258 staining.CAS increased the population of apoptotic cells, in a time- and concentration-dependent manner( 0.05). The results of FCM analysis after PI staining showed that CAS induced apoptosis in SW480 cells in time- and concentration-dependent manner( 0.05).Western Blotting analysis showed CAS up-regulated the expression of death receptor-5 (DR5) and inhibition activity of nuclear factor kappaB (NF-κB) ( 0.05).Conclusion CAS can inhibits the proliferation and induces apoptosis of human colon cancer SW480 cells in vitro and this action was associated with up-regulation of the expretion of the death receptor -5 (DR5) and inhibition of nuclear factor kappaB (NF-κB) activity. |