Potent cytotoxicity and induction of ROS-mediated genomic instability, mitochondrial dysfunction, and apoptosis by Y(2)O(3) NPs in Hep-G2 hepatic cancer cells

Y₂O₃纳米颗粒对Hep-G2肝癌细胞具有强效细胞毒性,并能诱导ROS介导的基因组不稳定、线粒体功能障碍和细胞凋亡。

阅读:2

Abstract

Hepatic cancer, one of the most prevalent and lethal cancers globally, remains a significant health challenge, with limited treatment options underscoring the urgent need for novel, more effective therapies. Yttrium oxide nanoparticles (Y(2)O(3) NPs) have attracted attention in nanomedicine due to their promising properties, including enhanced drug delivery, imaging capabilities, and therapeutic effects. However, the specific impact of Y(2)O(3) NPs on hepatic cancer is largely unexplored. Therefore, this study was conducted to assess the cytotoxic effects of Y(2)O(3) NPs on cell viability, reactive oxygen species (ROS) generation, genomic stability, mitochondrial integrity, and apoptosis induction in Hep-G2 hepatic cancer cells. The results from the SRB cytotoxicity assay demonstrated a strong concentration-dependent decrease in Hep-G2 cell viability, with a notably low half-maximal inhibitory concentration (IC50) value of 13.15 µg/ml. Exposure to the IC50 concentration of Y(2)O(3) NPs led to increased ROS generation, DNA damage induction, and loss of mitochondrial membrane potential. Furthermore, the expression of pro-apoptotic p53 and mitochondrial ND3 genes was significantly upregulated, while the anti-apoptotic Bcl-2 gene was markedly downregulated, triggering apoptosis in Hep-G2 cells after 72 h of exposure to Y(2)O(3) NPs. Collectively, these findings highlight the therapeutic potential of Y(2)O(3) NPs in hepatic cancer, emphasizing the need for further research to fully explore their efficacy as a treatment option for liver cancer.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。