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

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.

Automated summary

This study evaluated the therapeutic potential of erbium oxide nanoparticles (Er2O3-NPs) on human hepatocellular carcinoma (Hep-G2) cells. Exposure to Er2O3-NPs inhibited the growth of Hep-G2 cells and induced cell death in a concentration dependent manner. Er2O3-NPs also caused high levels of DNA damage and intracellular reactive oxygen species (ROS) production in Hep-G2 cells. Flow cytometry analysis revealed that Er2O3-NPs arrested the cell cycle of Hep-G2 cells at the G0/G1 phase and increased the number of cells in the apoptotic and necrotic phases. Furthermore, Er2O3-NPs upregulated the expression levels of apoptotic genes (p53 and Bax) and downregulated the expression level of the anti-apoptotic gene Bcl2 in Hep-G2 cells. In conclusion, Er2O3-NPs inhibit the proliferation of Hep-G2 cells and induce apoptosis through ROS generation, DNA damage, and alteration of apoptotic genes. Further in vitro and in vivo studies are recommended to explore the potential of using Er2O3-NPs in cancer treatment.