Lysosome-dependent necrosis specifically evoked in cancer cells by gold nanorods. (July 2017)

• Record Type: Journal Article
• Authors: Zhang, Fulei; Chen, Di; Wang, Ying; Zhang, Li; Dong, Wei; Dai, Jianxin; Jin, Chong; Dong, Xia; Sun, Yun; Zhao, He; Fan, Kexin; Liu, Hui; Chen, Bingdi; Zou, Hao; Li, Wei
• Is Part Of: Nanomedicine. Volume 12:Number 13(2017)
• Page Start: 1575
• Page End: 1589
• Publication Date: 2017-07
• Subjects: cathepsin B -- gold nanorods -- lysosome -- nanomedicine -- necrosis -- RIP1; Nanotechnology -- Periodicals; Medical technology -- Periodicals; Nanotechnology -- Therapeutic use -- Periodicals; 610.28
• DOI: 10.2217/nnm-2017-0126
• Languages: English
• ISSNs: 1743-5889

Abstract

Aim: This article aims to explain the necrosis mechanisms of cancer cells specifically induced by gold nanorods (GNRs).Methods: The intracellular route and location of GNRs, the interaction between GNRs and lysosome, lysosome damage, cathepsin B release, necrosis complex formation, receptor-interacting protein 1 and TNF-α expression were systematically investigated.Results: The GNRs with serum corona were internalized quickly by cancer cells and finally taken up by lysosomes. The GNRs damaged the lysosomal membrane, resulting in the leakage of cathepsin B, which promoted the activation of receptor-interacting protein 1 and necrosomes formation. Necrotic cells and their debris or ill cellular contents were engulfed by macrophages resulting in high-level release of TNF-α, which further confirmed necrosis.Conclusion: GNRs can specifically trigger lysosome-dependent necrosis in cancer cells.