ArticleNanomaterials (Basel, Switzerland)2021
Gold Nanoparticles and Graphene Oxide Flakes Enhance Cancer Cells' Phagocytosis through Granzyme-Perforin-Dependent Biomechanism.
Article in Nanomaterials (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 32 citations in OpenAlex.
- Promising antibiofilm formation: Liquid phase pulsed laser ablation synthesis of Graphene Oxide@Platinum core-shell nanoparticles.PloS one · 2024Article
- Gold Nanoparticles Enhancing Generation of ROS for Cs-137 Radiotherapy.Nanoscale research letters · 2022Article
- Green synthesized gold nanoparticles fromDrug delivery · 2022Article
- Copper Oxide Nanoparticle-Decorated Carbon Nanoparticle Composite Colloidal Preparation through Laser Ablation for Antimicrobial and Antiproliferative Actions against Breast Cancer Cell Line, MCF-7.BioMed research international · 2022Article
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Authors and funding
10 authors at 2 institutions in 4 countries.
Funding
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Abstract
The study aimed to investigate the roles of gold nanoparticles (GNPs) and graphene oxide flakes (GOFs) as phagocytosis enhancers against cancer cells. The nanomaterials were characterized through SEM and UV-VIS absorptions. The GNPs and GOFs increased the macrophages' phagocytosis ability in engulfing, thereby annihilating the cancer cells in both in vitro and in vivo conditions. The GNPs and GOFs augmented serine protease class apoptotic protein, granzyme, passing through the aquaporin class protein, perforin, with mediated delivery through the cell membrane site for the programmed, calibrated, and conditioned cancer cells killing. Additionally, protease inhibitor 3,4-dichloroisocoumarin (DCI) significantly reduced granzyme and perforin activities of macrophages. The results demonstrated that the GOFs and GNPs increased the activation of phagocytic cells as a promising strategy for controlling cancer cells by augmenting the cell mortality through the granzyme-perforin-dependent mechanism.
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