Induction of ROS mediated genomic instability, apoptosis and G0/G1 cell cycle arrest by erbium oxide nanoparticles in human hepatic Hep-G2 cancer cells

Abstract The remarkable physical and chemical characteristics of noble metal nanoparticles, such as high surface-to-volume ratio, broad optical properties, ease of assembly, surfactant and functional chemistry, have increased scientific interest in using erbium oxide nanoparticles (Er2O3-NPs) and ot...

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Main Authors: Gehan Safwat, Esraa S. M. Soliman, Hanan R. H. Mohamed
Format: Article
Language:English
Published: Nature Portfolio 2022-09-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-022-20830-3
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author Gehan Safwat
Esraa S. M. Soliman
Hanan R. H. Mohamed
author_facet Gehan Safwat
Esraa S. M. Soliman
Hanan R. H. Mohamed
author_sort Gehan Safwat
collection DOAJ
description Abstract The remarkable physical and chemical characteristics of noble metal nanoparticles, such as high surface-to-volume ratio, broad optical properties, ease of assembly, surfactant and functional chemistry, have increased scientific interest in using erbium oxide nanoparticles (Er2O3-NPs) and other noble metal nanostructures in cancer treatment. However, the therapeutic effect of Er2O3-NPs on hepatic cancer cells has not been studied. Therefore, the current study was conducted to estimate the therapeutic potential of Er2O3-NPs on human hepatocellular carcinoma (Hep-G2) cells. Exposure to Er2O3-NPs for 72 h inhibited growth and caused death of Hep-G2 cells in a concentration dependent manner. High DNA damage and extra-production of intracellular reactive oxygen species (ROS) were induced by Er2O3-NPs in Hep-G2 cells. As determined by flow cytometry, Er2O3-NPs arrested Hep-G2 cell cycle at the G0/G1 phase and markedly increased the number of Hep-G2 cells in the apoptotic and necrotic phases. Moreover, Er2O3-NPs caused simultaneous marked increases in expression levels of apoptotic (p53 and Bax) genes and decreased level of anti-apoptotic Bcl2 gene expression level in Hep-G2 cells. Thus it is concluded that Er2O3-NPs inhibit proliferation and trigger apoptosis of Hep-G2 cells through the extra ROS generation causing high DNA damage induction and alterations of apoptotic genes. Thus it is recommended that further in vitro and in vivo studies be carried out to study the possibility of using Er2O3-NPs in the treatment of cancer.
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spelling doaj.art-11e511b0c5484424884e6c37df8dcc452022-12-22T04:29:03ZengNature PortfolioScientific Reports2045-23222022-09-0112111010.1038/s41598-022-20830-3Induction of ROS mediated genomic instability, apoptosis and G0/G1 cell cycle arrest by erbium oxide nanoparticles in human hepatic Hep-G2 cancer cellsGehan Safwat0Esraa S. M. Soliman1Hanan R. H. Mohamed2Faculty of Biotechnology, October University for Modern Sciences and ArtsFaculty of Biotechnology, October University for Modern Sciences and ArtsZoology Department, Faculty of Science, Cairo UniversityAbstract The remarkable physical and chemical characteristics of noble metal nanoparticles, such as high surface-to-volume ratio, broad optical properties, ease of assembly, surfactant and functional chemistry, have increased scientific interest in using erbium oxide nanoparticles (Er2O3-NPs) and other noble metal nanostructures in cancer treatment. However, the therapeutic effect of Er2O3-NPs on hepatic cancer cells has not been studied. Therefore, the current study was conducted to estimate the therapeutic potential of Er2O3-NPs on human hepatocellular carcinoma (Hep-G2) cells. Exposure to Er2O3-NPs for 72 h inhibited growth and caused death of Hep-G2 cells in a concentration dependent manner. High DNA damage and extra-production of intracellular reactive oxygen species (ROS) were induced by Er2O3-NPs in Hep-G2 cells. As determined by flow cytometry, Er2O3-NPs arrested Hep-G2 cell cycle at the G0/G1 phase and markedly increased the number of Hep-G2 cells in the apoptotic and necrotic phases. Moreover, Er2O3-NPs caused simultaneous marked increases in expression levels of apoptotic (p53 and Bax) genes and decreased level of anti-apoptotic Bcl2 gene expression level in Hep-G2 cells. Thus it is concluded that Er2O3-NPs inhibit proliferation and trigger apoptosis of Hep-G2 cells through the extra ROS generation causing high DNA damage induction and alterations of apoptotic genes. Thus it is recommended that further in vitro and in vivo studies be carried out to study the possibility of using Er2O3-NPs in the treatment of cancer.https://doi.org/10.1038/s41598-022-20830-3
spellingShingle Gehan Safwat
Esraa S. M. Soliman
Hanan R. H. Mohamed
Induction of ROS mediated genomic instability, apoptosis and G0/G1 cell cycle arrest by erbium oxide nanoparticles in human hepatic Hep-G2 cancer cells
Scientific Reports
title Induction of ROS mediated genomic instability, apoptosis and G0/G1 cell cycle arrest by erbium oxide nanoparticles in human hepatic Hep-G2 cancer cells
title_full Induction of ROS mediated genomic instability, apoptosis and G0/G1 cell cycle arrest by erbium oxide nanoparticles in human hepatic Hep-G2 cancer cells
title_fullStr Induction of ROS mediated genomic instability, apoptosis and G0/G1 cell cycle arrest by erbium oxide nanoparticles in human hepatic Hep-G2 cancer cells
title_full_unstemmed Induction of ROS mediated genomic instability, apoptosis and G0/G1 cell cycle arrest by erbium oxide nanoparticles in human hepatic Hep-G2 cancer cells
title_short Induction of ROS mediated genomic instability, apoptosis and G0/G1 cell cycle arrest by erbium oxide nanoparticles in human hepatic Hep-G2 cancer cells
title_sort induction of ros mediated genomic instability apoptosis and g0 g1 cell cycle arrest by erbium oxide nanoparticles in human hepatic hep g2 cancer cells
url https://doi.org/10.1038/s41598-022-20830-3
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AT esraasmsoliman inductionofrosmediatedgenomicinstabilityapoptosisandg0g1cellcyclearrestbyerbiumoxidenanoparticlesinhumanhepatichepg2cancercells
AT hananrhmohamed inductionofrosmediatedgenomicinstabilityapoptosisandg0g1cellcyclearrestbyerbiumoxidenanoparticlesinhumanhepatichepg2cancercells