Dracorhodin perchlorate, an anthocyanin red pigment, induces human melanoma 
A375-S2 cell death through the apoptotic pathway. Caspase-3, -8, -9, and -10 
inhibitors partially reversed the cell death induced by dracorhodin perchlorate. 
Caspase-3 and -8 were activated, followed by the degradation of caspase-3 
substrates, the inhibitor of caspase-activated DNase, and poly-(ADP-ribose) 
polymerase. Dracorhodin perchlorate upregulated the expression ratio of 
Bax/Bcl-2 and significantly increased the expression of p53 and p21(WAF1) 
proteins. The cell death was partially reduced by the mitogen-activated protein 
kinase c-JUN NH2-terminal protein kinase (JNK MAPK) inhibitor (SP600125) and p38 
MAPK inhibitor (SB 203580), while the MEK inhibitor (PD98059) augmented cell 
death; the drug induced sustained phosphorylation of JNK and p38 MAPK. Moreover, 
the Fas agonistic antibody CH-11 has a synergistic effect with dracorhodin 
perchlorate. The phoshatidylinositol 3-kinase (PI3-K) family inhibitor wortmanin 
and tyrosine kinase inhibitor genistein rescued the viability loss induced by 
dracohodin perchlorate. Taken together, dracorhodin perchlorate induces 
apoptosis in A375-S2 cells via accumulation of p53, alters the Bax/Bcl-2 ratio, 
and activates caspases and p38/JNK MAPKs.