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Although the remarkable anti tumor effect of tumor necrosis factor (TNF-α) and the essential role in diverse cellular and immunological properties have been evidenced, the clinical use of TNF-α is hindered due to its toxicity. Our study was aimed to develop a new drug delivery system by binding pygelated gold nanoparticles (50 nm) with TNF-α and then investigate the anticancer activity against AMJ13 cell line. The binding of these compounds were confirmed and characterized using ultraviolet-visible spectroscopy (UV-Vis), scanning electrone microscope (SEM), and transmision electrone microscope (TEM). Varios parameters in vitro were used to examine the anticancer activity of each compound against AMJ13 cell line. Gold nanoparticles (GNPs) and TNFα-GNPs were found to exert cell growth arrest against the cancer cell line. The anti-proliferative effect of these compounds was due to cell death and inducing apoptosis as confirmed by using 4', 6-Diamidino-2-phenylindole (DAPI) fluorescent assay, flow cytometry assay, and finally mitochondrial membrane potential (MMP) staining, Real-time polymerase chanin reaction (RT-PCR) was used to detect changes in the expression of p53 protein. In addition, we studied the effect of drug delivery system on body weight on mice. In conclusion, the results of this study demonstrated that the TNFα-GNPs inhibited AMJ13 cells proliferation, resulting in apoptosis during novel pathway that involved mitochondrial damage and up-reglulated p53. Taken together, the results suggested that the TNFα loaded GNPs could be a promising therapy protocol for cancer cells and could be used for wide medical applications and offer new drug recompensing a chemotherapy drug.


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TNF-α Loaded on Gold Nanoparticles as a Good Therapeutic Agent against Breast Cancer AMJ13 Cells

Show Author's information Noor Abood1Majid Jabir2( )Haider Kadhim3
Medical Laboratory Techniques, Al-Mamoon University College Baghdad, Iraq
Division of Biotechnology, Department of Applied Science, University of Technology, Baghdad, Iraq
Department of Micrbiology, University of Al-nahrain, Baghdad, Iraq

Abstract

Although the remarkable anti tumor effect of tumor necrosis factor (TNF-α) and the essential role in diverse cellular and immunological properties have been evidenced, the clinical use of TNF-α is hindered due to its toxicity. Our study was aimed to develop a new drug delivery system by binding pygelated gold nanoparticles (50 nm) with TNF-α and then investigate the anticancer activity against AMJ13 cell line. The binding of these compounds were confirmed and characterized using ultraviolet-visible spectroscopy (UV-Vis), scanning electrone microscope (SEM), and transmision electrone microscope (TEM). Varios parameters in vitro were used to examine the anticancer activity of each compound against AMJ13 cell line. Gold nanoparticles (GNPs) and TNFα-GNPs were found to exert cell growth arrest against the cancer cell line. The anti-proliferative effect of these compounds was due to cell death and inducing apoptosis as confirmed by using 4', 6-Diamidino-2-phenylindole (DAPI) fluorescent assay, flow cytometry assay, and finally mitochondrial membrane potential (MMP) staining, Real-time polymerase chanin reaction (RT-PCR) was used to detect changes in the expression of p53 protein. In addition, we studied the effect of drug delivery system on body weight on mice. In conclusion, the results of this study demonstrated that the TNFα-GNPs inhibited AMJ13 cells proliferation, resulting in apoptosis during novel pathway that involved mitochondrial damage and up-reglulated p53. Taken together, the results suggested that the TNFα loaded GNPs could be a promising therapy protocol for cancer cells and could be used for wide medical applications and offer new drug recompensing a chemotherapy drug.

Keywords: Cytotoxicity, TNF-α, GNPs, TNF loaded GNPs, AMJ13 cells, MMP, p53 expresion

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Publication history
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Publication history

Received: 14 March 2020
Accepted: 03 July 2020
Published: 10 September 2020
Issue date: September 2020

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© Noor Abood, Majid Jabir, and Haider Kadhim.

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This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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