Scientific Reports (May 2024)

Biosynthesized BiFe2O4@Ag nanoparticles mediated Scenedesmus obliquus induce apoptosis in AGS gastric cancer cell line

  • Hossein Shamsi,
  • Reza Yari,
  • Ali Salehzadeh

DOI
https://doi.org/10.1038/s41598-024-57157-0
Journal volume & issue
Vol. 14, no. 1
pp. 1 – 11

Abstract

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Abstract The use of magnetic metal nanoparticles has been considered in cancer treatment studies. In this study, BiFe2O4@Ag nanoparticles were synthesized biologically by Scenedesmus obliquus for the first time and their anticancer mechanism in a gastric cancer cell line was characterized. The physicochemical properties of the nanoparticles were evaluated by fourier transform infrared spectroscopy (FT-IR), X-ray diffraction (XRD), energy-dispersive X-ray spectroscopy (EDS), scanning electron microscopy (SEM), transmission electron microscopy (TEM), dynamic Light Scattering (DLS), and zeta potential analyses. Cell viability and nuclear damage were investigated by the MTT and Hoechst staining assays, respectively. Flow cytometry analysis was performed to determine the frequency of the necrotic and apoptotic cells as well as cell cycle analysis of the nanoparticles-treated cells. Physicochemical characterization showed that the synthesized particles were spherical, without impurities, in a size range of 38–83 nm, with DLS size and zeta potential of 295.7 nm and -27.7 mV, respectively. BiFe2O4@Ag nanoparticles were considerably more toxic for the gastric cancer cells (AGS cell line) than HEK293 normal cells with IC50 of 67 and 117 µg/ml, respectively. Treatment of AGS cells with the nanoparticles led to a remarkable increase in the percentage of late apoptosis (38.5 folds) and cell necrosis (13.4 folds) and caused cell cycle arrest, mainly at the S phase. Also, nuclear fragmentation and apoptotic bodies were observed in the gastric cancer cells treated with the nanoparticles. This study represents BiFe2O4@Ag as a novel anticancer candidate against gastric cancer that can induce cell apoptosis through DNA damage and inhibition of cell cycle progression.

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