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Biogenic selenium nanoparticles induce ROS-mediated necroptosis in PC-3 cancer cells through TNF activation
Praveen Sonkusre1, Swaranjit Singh Cameotra2
1Institute of Microbial Technology, Sector 39 A, Chandigarh, 160036, India.
Background:
Selenium is well documented to inhibit cancer at higher doses; however, the mechanism behind this inhibition varies widely depending on the cell type and selenium species. Previously, we have demonstrated that Bacillus licheniformis JS2 derived biogenic selenium nanoparticles (SeNPs) induce non-apoptotic cell death in prostate adenocarcinoma cell line, PC-3, at a minimal concentration of 2 µg Se/ml, without causing toxicity to the primary cells. However, the mechanism behind its anticancer activity was elusive.
Results:
Our results have shown that these SeNPs at a concentration of 2 µg Se/ml were able to induce reactive oxygen species (ROS) mediated necroptosis in PC-3 cells by gaining cellular internalization. Real-time qPCR analysis showed increased expression of necroptosis associated tumor necrotic factor (TNF) and interferon regulatory factor 1 (IRF1). An increased expression of RIP1 protein was also observed at the translational level upon SeNP treatment. Moreover, the cell viability was significantly increased in the presence of necroptosis inhibitor, Necrostatin-1.
Conclusion:
Data suggest that our biogenic SeNPs induce cell death in PC-3 cells by the ROS-mediated activation of necroptosis, independent to RIP3 and MLKL, regulated by a RIP1 kinase.
Insights
Biogenic selenium nanoparticles (SeNPs) induce programmed cell death (necroptosis) in prostate cancer cells. This targeted cell death is mediated by reactive oxygen species (ROS) and offers a novel therapeutic strategy.
Area of Science:
- Nanotechnology
- Biochemistry
- Oncology
Background:
- Selenium nanoparticles (SeNPs) show anticancer properties, but mechanisms are cell-type dependent.
- Biogenic SeNPs from Bacillus licheniformis JS2 induce non-apoptotic cell death in PC-3 prostate cancer cells at 2 µg Se/ml.
- Previous studies identified SeNPs' anticancer effect but not the precise mechanism.
Purpose of the Study:
- To elucidate the mechanism by which biogenic SeNPs induce cell death in PC-3 cells.
- To investigate the role of reactive oxygen species (ROS) and specific cell death pathways.
Main Methods:
- Cellular internalization studies of SeNPs.
- Real-time quantitative polymerase chain reaction (qPCR) to analyze gene expression.
- Western blot analysis for protein expression.
- Cell viability assays with necroptosis inhibitors.
Main Results:
- SeNPs at 2 µg Se/ml induced reactive oxygen species (ROS)-mediated necroptosis in PC-3 cells.
- Increased expression of tumor necrosis factor (TNF) and interferon regulatory factor 1 (IRF1) was observed.
- RIP1 protein expression increased, and necroptosis inhibition significantly reduced cell death.
Conclusions:
- Biogenic SeNPs trigger cell death in PC-3 cells via ROS-mediated necroptosis.
- The pathway is regulated by RIP1 kinase, independent of RIP3 and MLKL.
- This suggests a novel therapeutic approach for prostate cancer using SeNPs.
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