Effects and mechanisms of emodin on cell death in human lung squamous cellcarcinoma

1 Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is an active component fr om the root and rhizome of Rheum palmation that has been reported to exhibi t antitumour effects, but the mechanism is not known, The study investigate d the effects and mechanisms of emodin-induced cell death in human lung squ amous carcinoma cell line CH27. 2 Emodin (50 muM)-induced CH27 cell apoptosis was confirmed by cell morphol ogical change, sub-G(1) formation in flow cytometry analysis, viability ass ay and degradation of focal adhesion kinase in this study. 3 Emodin-induced apoptosis of CH27 cells does not involve modulation of end ogenous Bcl-X-L protein expression, but appears to be associated with the i ncreased expression of cellular Bak and Bax proteins. This study also demon strated the translocation of Bak and Bax from cytosolic to particulate frac tions. 4 This study has shown that emodin-treated CH27 cells revealed the increase s in the relative abundance of cytochrome c for the indicated time interval s in cytosolic fraction. 5 This study demonstrates that the activation of caspase-3, caspase-9 and c aspase-8 is an important determinant of apoptotic death induced by emodin. 6 These results suggested that emodin induces CH27 cell death by Bax death pathway and Fas pathway.