Modulation of gold(III) porphyrin 1a-induced apoptosis by mitogen-activated protein kinase signaling pathways

摘要: Gold(III) porphyrin 1a is a novel gold(III) complex with selective anticancer effect in number of human carcinoma cell lines. We have previously shown that mediated mitochondrial transmembrane potential (ΔΨm) depletion, leading to cytochrome c release, nucleus translocation apoptosis-inducing factor (AIF), and generation reactive oxygen species (ROS). The current study addressed 1a-induced phosphoproteome alterations modulation death by the mitogen-activated protein kinase (MAPK) family proteins. ERK p38MAPK were transiently activated upon treatment. Inhibition phosphorylation rescued upstream caspase activation. Attenuation ΔΨm was primary phosphorylation. Further functional proteomic suggested differential regulation phosphotyrosine proteins related activation signal transduction cascade. In summary, modulated downstream mitochondria, multiple also involved this process. These results promising agent directed toward mitochondria.