ZnPcS2P2-basedPhotodynamicTherapyInducesMitochondria-dependentApoptosisinK562Cells

<正> Mitochondria play a key role in the regulation of apoptosis induced by numerous antitumorchemotherapeutic and other toxic agents.Photodynamic therapy （PDT） exerts significant cellular killingefficacy through either an apoptotic or necrotic cell death pathway.This study investigated the mechanismunderlying the killing effects of a novel amphipathic photosensitizer [di-sulfonated di-phthalimidomethylphthalocyanine zinc （ZnPcS2P2）]-mediated photodynamic therapy （ZnPcS2P2-PDT） on K562 cells.Apoptosiswas evident in the post-PDT cells through the TdT-mediated dUTP nick end labeling （TUNEL） method andDNA fragmentation assay.After ZnPcS2P2-PDT,K562 cells underwent mitochondria-dependent apoptosisas evidenced by the release of cytochrome c from mitochondria into cytosol,accompanied by mitochondrialmembrane potential （ΔΨm） reduction,indicating the opening of the mitochondrial permeability transitionpore （PTP）.The activities of protease from the caspase family and caspase-3 were also significantly elevated.Furthermore,ZnPcS2P2-PDT down-regulated the expression of chimaeric Bcr-Abl oncoprotein,which isthe molecular hallmark of chronic myelogenous leukemia （CML）.