Lysosome-mitochondria-mediated apoptosis specifically evoked in cancer cells induced by gold nanorods

• Published in: Nanomedicine (London, England) England), 2016-08, Vol.11 (15), p.1993-2006
• Main Authors: Zhang, Fulei, Zhu, Xiandi, Gong, Jing, Sun, Yun, Chen, Di, Wang, Jie, Wang, Ying, Guo, Mengfang, Li, Wei
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Apoptosis - drug effects; Biomedical materials; Cancer therapies; Caspase 3 - metabolism; Caspase 9 - metabolism; Cell Line, Tumor; Cell Survival; Chemotherapy; Cricetulus; Cytochrome; Enzymes; Gold - chemistry; Gold - therapeutic use; gold nanorods; Humans; lysosome; Lysosomes - metabolism; Medical prognosis; Membrane Potential, Mitochondrial; Mice; Mitochondria; Mitochondria - metabolism; mitochondrion; Nanomaterials; Nanotubes - chemistry; Particle Size; Quantum dots; Transmission electron microscopy
• ISSN: 1743-5889; 1748-6963
• DOI: 10.2217/nnm-2016-0139

The main aim of this article is to explain the apoptosis mechanisms of cancer cells specifically triggered by gold nanorods (GNRs). GNRs were synthesized and optimized, the lysosome damage, cathepsin D, mitochondrial membrane potential, caspase-9, cleaved caspase-9, caspase-3 and intracellular GNRs location related to apoptosis was systematically evaluated. GNRs specifically induce cancer cell apoptosis while posing a negligible impact on normal cells. After incubation with GNRs, the lysosomal permeability in cancer cells as indicated by cathepsin D was markedly higher than that in normal cells and resulted in an obvious decrease in mitochondrial membrane potential. Western blot analysis further confirmed that apoptosis occurred through caspase-9 and caspase-3 activation following mitochondrial damage. Transmission electron microscope images showed that GNRs did not appear in most of the damaged mitochondria but mainly accumulated in lysosomes. These findings indicated that GNR-induced apoptosis specifically in cancer cells by affecting lysosomes and mitochondria.