Gold Nanoparticles and Graphene Oxide Flakes Enhance Cancer Cells' Phagocytosis through Granzyme-Perforin-Dependent Biomechanism.

Mohsen S Al-Omar,Ghassan M Sulaiman,Zainab J Taqi,Khawla S Khashan,Esraa Karsh,Hamdoon A Mohammed,Majid Jabir,Riaz A Khan,Rua Kadhim,Salman A A Mohammed

doi:10.3390/nano11061382

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.

Highlights

Macrophages are cells of the immune system that are characterized by plasticity and heterogeneity [1]
The current study demonstrates phagocytic cells’ activity against cancer cells, mediated by gold nanoparticles (GNPs) and graphene oxide flakes (GOFs) (Figure 1)
The results showed a significant increase in the CD11b+/eFlour 670+ cell gated CD11b+ cells and measured percentage of bone marrow-derived macrophages (BMDMs) with double staining population in BMDMs the pre-treated with GNPs and GOFs compared with the control group, (Figure 5)

Summary

Introduction

Macrophages are cells of the immune system that are characterized by plasticity and heterogeneity [1]. Macrophages show one of the most potent reactions characterized by their effective roles in host defense modulation, inflammation, and homeostasis [5]. These cells can control the initiation and resolution phases for innate and adaptive immune responses due to their potent capabilities to engulf bacterial cells, present antigens, and secrete cytokines [6]. The function of these cells is critically dependent on their polarization and reprogramming states. A reversal of the phenotype can lead to the already polarized cell’s reprogramming [4]

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