Zinc oxide nanoparticles induce toxic responses in human neuroblastoma SHSY5Y cells in a size-dependent manner

Liu, Jia; Kang, Youjeong; Yin, Suhan; Song, Bin; Wei, Limin; Chen, Liangjiao; Shao, Longquan

doi:10.2147/ijn.s149070

Cited by 96 publications

(53 citation statements)

References 65 publications

(79 reference statements)

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“…Apigenin-functionalized ultra-small PtNPs induced cytotoxicity in a dose-dependent manner by reducing cell viability and proliferation in human monocytic THP-1 cells [48]. Similarly, zinc oxide nanoparticles induced cell death in dose-and time-dependent manners in SH-SY5Y cells [57], and tangeretin-assisted PtNPs showed dose-dependent cytotoxicity against human bone OS epithelial cells [49]. Altogether, beta carotene-functionalized PtNPs have significant cytotoxic effects against human neuroblastoma cells, which are mediated by the reduction in cell viability and cell proliferation.…”

Section: Dose-dependent Effects Of Ptnps Ra and Cisplatin On The VImentioning

confidence: 98%

Anticancer Properties of Platinum Nanoparticles and Retinoic Acid: Combination Therapy for the Treatment of Human Neuroblastoma Cancer

Gurunathan

Jeyaraj

Kang

et al. 2020

IJMS

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Neuroblastoma is the most common extracranial solid tumor in childhood. The different treatments available for neuroblastoma are challenged by high rates of resistance, recurrence, and progression, most notably in advanced cases and highly malignant tumors. Therefore, the development of more targeted therapies, which are biocompatible and without undesired side effects, is highly desirable. The mechanisms of actions of platinum nanoparticles (PtNPs) and retinoic acid (RA) in neuroblastoma have remained unclear. In this study, the anticancer effects of PtNPs and RA on neuroblastoma were assessed. We demonstrated that treatment of SH-SY5Y cells with the combination of PtNPs and RA resulted in improved anticancer effects. The anticancer effects of the two compounds were mediated by cytotoxicity, oxidative stress (OS), mitochondrial dysfunction, endoplasmic reticulum stress (ERS), and apoptosis-associated networks. Cytotoxicity was confirmed by leakage of lactate dehydrogenase (LDH) and intracellular protease, and oxidative stress increased the level of reactive oxygen species (ROS), 4-hydroxynonenal (HNE), malondialdehyde (MDA), and nitric oxide (NO), and protein carbonyl content (PCC). The combination of PtNPs and RA caused mitochondrial dysfunction by decreasing the mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) content, number of mitochondria, and expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). Endoplasmic reticulum-mediated stress and apoptosis were confirmed by upregulation of protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1 (IRE1), activating transcription factor 6 (ATF6), activating transcription factor 4 (ATF4), p53, Bax, and caspase-3 and down regulation of B-cell lymphoma 2 (BCl-2). PtNPs and RA induced apoptosis, and oxidative DNA damage was evident by the accumulation of 8-hydroxy-2-deoxyguanosine (8-OHdG) and 8-hydroxyguanosine (8-OHG). Finally, PtNPs and RA increased the differentiation and expression of differentiation markers. Differentiated SH-SY5Y cells pre-treated with PtNPs or RA or the combination of both were more sensitive to the cytotoxic effect of cisplatin than undifferentiated cells. To our knowledge, this is the first study to demonstrate the effect of the combination of PtNPs and RA in neuroblastoma cells. PtNPs may be a potential preconditioning or adjuvant compound in chemotherapeutic treatment. The results of this study provide a rationale for clinical evaluation of the combination of PtNPs and RA for the treatment of children suffering from high-risk neuroblastoma.

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Section: Dose-dependent Effects Of Ptnps Ra and Cisplatin On The VImentioning

confidence: 98%

Anticancer Properties of Platinum Nanoparticles and Retinoic Acid: Combination Therapy for the Treatment of Human Neuroblastoma Cancer

Gurunathan

Jeyaraj

Kang

et al. 2020

IJMS

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“…Reproduced from[143] under the Creative Commons Attribution.4.1.2. Cancerous CellsNano-ZnO materials have been reported to attack multiple cancer cell lines based on cytotoxic assay results[50,126,[147][148][149][150][151][152][153][154][155][156][157][158][159][160][161][162]. Very recently, Hussain et al synthesized spherical ZnO NPs (90 nm) from Pandanus odorifer leaf extract and zinc acetate dihydrate.…”

mentioning

confidence: 99%

Interactions of Zinc Oxide Nanostructures with Mammalian Cells: Cytotoxicity and Photocatalytic Toxicity

Liao

Jin

et al. 2020

IJMS

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This article presents a state-of-the-art review and analysis of literature studies on the morphological structure, fabrication, cytotoxicity, and photocatalytic toxicity of zinc oxide nanostructures (nZnO) of mammalian cells. nZnO with different morphologies, e.g., quantum dots, nanoparticles, nanorods, and nanotetrapods are toxic to a wide variety of mammalian cell lines due to in vitro cell–material interactions. Several mechanisms responsible for in vitro cytotoxicity have been proposed. These include the penetration of nZnO into the cytoplasm, generating reactive oxygen species (ROS) that degrade mitochondrial function, induce endoplasmic reticulum stress, and damage deoxyribonucleic acid (DNA), lipid, and protein molecules. Otherwise, nZnO dissolve extracellularly into zinc ions and the subsequent diffusion of ions into the cytoplasm can create ROS. Furthermore, internalization of nZnO and localization in acidic lysosomes result in their dissolution into zinc ions, producing ROS too in cytoplasm. These ROS-mediated responses induce caspase-dependent apoptosis via the activation of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), CCAAT/enhancer-binding protein homologous protein (chop), and phosphoprotein p53 gene expressions. In vivo studies on a mouse model reveal the adverse impacts of nZnO on internal organs through different administration routes. The administration of ZnO nanoparticles into mice via intraperitoneal instillation and intravenous injection facilitates their accumulation in target organs, such as the liver, spleen, and lung. ZnO is a semiconductor with a large bandgap showing photocatalytic behavior under ultraviolet (UV) light irradiation. As such, photogenerated electron–hole pairs react with adsorbed oxygen and water molecules to produce ROS. So, the ROS-mediated selective killing for human tumor cells is beneficial for cancer treatment in photodynamic therapy. The photoinduced effects of noble metal doped nZnO for creating ROS under UV and visible light for killing cancer cells are also addressed.

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“…However, another study showed that silica NPs (50 nm) induced higher apoptosis rates of HepG2 cells than did silica NPs (20 nm) [60]. ZnO NPs (49.4 nm) induced higher apoptosis rates of human neuroblastoma SHSY5Y cells than did ZnO NPs (90.8 nm) [167]. The translocation of Bax from the cytoplasm to mitochondria is a crucial step in apoptosis.…”

Section: The Impact Of Np Physicochemical Properties On Apoptosismentioning

confidence: 98%

The Rational Design and Biological Mechanisms of Nanoradiosensitizers

2020

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Radiotherapy (RT) has been widely used for cancer treatment. However, the intrinsic drawbacks of RT, such as radiotoxicity in normal tissues and tumor radioresistance, promoted the development of radiosensitizers. To date, various kinds of nanoparticles have been found to act as radiosensitizers in cancer radiotherapy. This review focuses on the current state of nanoradiosensitizers, especially the related biological mechanisms, and the key design strategies for generating nanoradiosensitizers. The regulation of oxidative stress, DNA damage, the cell cycle, autophagy and apoptosis by nanoradiosensitizers in vitro and in vivo is highlighted, which may guide the rational design of therapeutics for tumor radiosensitization.

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Zinc oxide nanoparticles induce toxic responses in human neuroblastoma SHSY5Y cells in a size-dependent manner

Cited by 96 publications

References 65 publications

Anticancer Properties of Platinum Nanoparticles and Retinoic Acid: Combination Therapy for the Treatment of Human Neuroblastoma Cancer

Anticancer Properties of Platinum Nanoparticles and Retinoic Acid: Combination Therapy for the Treatment of Human Neuroblastoma Cancer

Interactions of Zinc Oxide Nanostructures with Mammalian Cells: Cytotoxicity and Photocatalytic Toxicity

The Rational Design and Biological Mechanisms of Nanoradiosensitizers

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