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Dual role of oxidative stress-JNK activation in autophagy and apoptosis induced by nickel oxide nanoparticles in human cancer cells.

Free radical biology & medicine (2020-05-01)
Yik-Lam Cho, Hayden Weng Siong Tan, Quaiser Saquib, Yi Ren, Javed Ahmad, Rizwan Wahab, Weifeng He, Boon-Huat Bay, Han-Ming Shen
ABSTRACT

Nickel oxide nanoparticles (NiO-NPs) are an important group of nanoparticles with increasing applications in many aspects of industry. At present, there is evidence demonstrating the cytotoxic characteristics of NiO-NPs, while the involvement of autophagy in the cytotoxicity of NiO-NPs has not been reported. In this study, we aimed to study the role of autophagy in the cytotoxicity of NiO-NPs and the underlying regulatory mechanisms. First, we provided evidence that NiO-NPs induce autophagy in human cancer cells. Second, we found that the enhanced autophagic flux by NiO-NPs via the generation of intracellular reactive oxygen species (ROS) from mitochondria and the subsequent activation of the JNK pathway. Third, we demonstrated that the activation of JNK is a main force in mediating NiO-NPs-induced apoptosis. Finally, we demonstrated that the autophagic response plays an important protective role against the cytotoxic effect of NiO-NPs. Therefore, this study identifies the dual role of oxidative stress-JNK activation in the biological effects of NiO-NPs via promoting autophagy and mediating apoptosis. Understanding the protective role of autophagy and the underlying mechanism is important for the potential application of NiO-NPs in the biomedical industry.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Cobalt(II,III) oxide, nanopowder, <50 nm particle size (TEM), 99.5% trace metals basis
Sigma-Aldrich
Amyloid Protein Non-Aβ Component, ≥80% (HPLC)

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