EtBr-induced selective degradation of mitochondria occurs via autophagy

Abstract

Recent studies have implicated autophagy in numerous cellular responses to stress. During the establishment of human lung cancer cell lines without mitochondrial DNA, a significant depopulation of mitochondria occurred that was accompanied by the loss of the mitochondrial membrane potential. Notably, we observed autophagy in ethidium bromide (EtBr)-induced mitochondrial degradation. In the present study, we confirmed the involvement of autophagy in mitochondrial degradation after exposure to a low concentration of EtBr. Lung cancer cells undergoing mitochondrial autophagy exhibited a slower growth rate in vitro and in vivo. Furthermore, the degradation was mediated by the class III phosphatidylinositol 3-kinase (PI3K)-Beclin-1 complex. These findings indicate that autophagy is responsible for EtBr-induced mitochondrial degradation via the PI3K-Beclin-1 signaling pathway.