Sono-synthesis approach improves anticancer activity of ZnO nanoparticles: reactive oxygen species depletion for killing human osteosarcoma cells

Nanomedicine ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. 657-671
Author(s):  
Mansoureh Parsa ◽  
Mohammad H Entezari ◽  
Azadeh Meshkini
Keyword(s):  
Reactive Oxygen Species ◽  
Anticancer Activity ◽  
Zno Nanoparticles ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Zno Nps ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Tumor Selectivity ◽  
Biological Tests

Aim: To investigate the effect of ultrasound during the synthesis of ZnO nanoparticles (NPs) on their anticancer activity. Materials & methods: ZnO NPs were synthesized in the presence and absence of ultrasonic irradiation. Biological tests were performed on human osteosarcoma cancer cells (Saos-2). Results: The sono-synthesized sample indicated higher cytotoxicity than the conventional one. (IC50 = 16.48 ± 0.41 μg/ml for sonochemical ZnO; 26.96 ± 0.33 μg/ml for conventional ZnO). Both sonochemical and conventional samples acted like antioxidants and reduced intracellular reactive oxygen species level. This reduction was more significant in cells treated with the sono-synthesized sample. The sono-synthesized ZnO NPs showed more tumor selectivity than the conventional sample. Conclusion: Sono-synthesis of ZnO NPs by a bath sonicator could improve their anticancer activity.

scholarly journals Phyllanthus urinariaInduces Apoptosis in Human Osteosarcoma 143B Cells via Activation of Fas/FasL- and Mitochondria-Mediated Pathways

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Hsin-Yi Wu ◽  
Tsu-Kung Lin ◽  
Hsiao-Mei Kuo ◽  
Ya-Ling Huang ◽  
Chia-Wei Liou ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Extrinsic Pathway ◽  
Membrane Potential Change ◽  
Therapeutic Modalities ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Ligand Expression

Phyllanthus urinaria (P. urinaria), in this study, was used for the treatment of human osteosarcoma cells, which is one of the tough malignancies with few therapeutic modalities. Herein, we demonstrated thatP. urinariainhibited human osteosarcoma 143B cells growth through an apoptotic extrinsic pathway to activate Fas receptor/ligand expression. Both intracellular and mitochondrial reactive oxygen species were increased to lead to alterations of mitochondrial membrane permeability and Bcl-2 family including upregulation of Bid, tBid, and Bax and downregulation of Bcl-2.P. urinariatriggered an intrinsic pathway and amplified the caspase cascade to induce apoptosis of 143B cells. However, upregulation of both intracellular and mitochondrial reactive oxygen species and the sequential membrane potential change were less pronounced in the mitochondrial respiratory-defective 143Bρ0cells compared with the 143B cells. This study offers the evidence that mitochondria are essential for the anticancer mechanism induced byP. urinariathrough both extrinsic and intrinsic pathways.

scholarly journals Parthenolide Induces Reactive Oxygen Species-Mediated Autophagic Cell Death in Human Osteosarcoma Cells

2016 ◽  
Vol 40 (1-2) ◽  
pp. 146-154 ◽  
Author(s):  
Chen Yang ◽  
Qing Ou Yang ◽  
Qing-Jie Kong ◽  
Wen Yuan ◽  
Yue-Ping Ou Yang
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Annexin V ◽  
Pharmacological Action ◽  
Autophagic Cell Death ◽  
Oxygen Species ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

Background and Aim: Osteosarcoma is a devastating tumor of bone, primarily affecting adolescents. Parthenolide, a naturally occurring small molecule that interferes with NF-κB signaling, has recently attracted considerable attention because of its pharmacological action involving anti-cancer effects. However, the mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. Methods: In this study, the effects of parthenolide were evaluated and characterized in human osteosarcoma cancer cell. Cell viability was assessed by CCK-8. Apoptosis was assessed by Annexin V-FITC/PI Flow cytometry assay. Relative quantitative real-time PCR and western blot were used to determine the expressions of genes and proteins. Results: Our results suggest that parthenolide did not cause caspase-dependent cell death in osteosarcoma cancer cells, as indicated by the absence of significant early apoptosis as well as caspase-3 cleavage. Instead, parthenolide increased the autophagy and mitophagy, as characterized by increased PINK1 and Parkin translocation to mitochondria and enhanced autophagy proteins. The induction of autophagy by parthenolide was associated with the increase of reactive oxygen species (ROS). ROS antioxidants N-acetylcysteine (NAC) attenuated parthenolide-induced autophagy activity. Conclusions: Our findings unveil a novel mechanism of drug action by parthenolide in osteosarcoma cancer cells and suggest a potential value of treating osteosarcoma cancer through a caspase-independent autophagic cell death by ROS activation.

scholarly journals Marine Antimicrobial Peptide TP4 Exerts Anticancer Effects on Human Synovial Sarcoma Cells via Calcium Overload, Reactive Oxygen Species Production and Mitochondrial Hyperpolarization

Marine Drugs ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 93
Author(s):  
Bor-Chyuan Su ◽  
Giun-Yi Hung ◽  
Yun-Chieh Tu ◽  
Wei-Chen Yeh ◽  
Meng-Chieh Lin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Antimicrobial Peptide ◽  
Anticancer Activity ◽  
Synovial Sarcoma ◽  
Uncoupling Protein ◽  
Reactive Oxygen ◽  
Calcium Overload ◽  
Oxygen Species ◽  
Sarcoma Cells

Synovial sarcoma is a rare but aggressive soft-tissue sarcoma associated with translocation t(X;18). Metastasis occurs in approximately 50% of all patients, and curative outcomes are difficult to achieve in this group. Since the efficacies of current therapeutic approaches for metastatic synovial sarcoma remain limited, new therapeutic agents are urgently needed. Tilapia piscidin 4 (TP4), a marine antimicrobial peptide, is known to exhibit multiple biological functions, including anti-bacterial, wound-healing, immunomodulatory, and anticancer activities. In the present study, we assessed the anticancer activity of TP4 in human synovial sarcoma cells and determined the underlying mechanisms. We first demonstrated that TP4 can induce necrotic cell death in human synovial sarcoma AsKa-SS and SW982 cells lines. In addition, we saw that TP4 initiates reactive oxygen species (ROS) production and downregulates antioxidant proteins, such as uncoupling protein-2, superoxide dismutase (SOD)-1, and SOD-2. Moreover, TP4-induced mitochondrial hyperpolarization is followed by elevation of mitochondrial ROS. Calcium overload is also triggered by TP4, and cell death can be attenuated by a necrosis inhibitor, ROS scavenger or calcium chelator. In our experiments, TP4 displayed strong anticancer activity in human synovial sarcoma cells by disrupting oxidative status, promoting mitochondrial hyperpolarization and causing calcium overload.

Sign in / Sign up

Export Citation Format

Share Document