期刊
JOURNAL OF NANOBIOTECHNOLOGY
卷 15, 期 -, 页码 -出版社
BMC
DOI: 10.1186/s12951-017-0276-3
关键词
Bacillus licheniformis JS2; Biogenic selenium nanoparticles; PC-3; TNF; IRF1; Necroptosis; ROS; RIP1
资金
- CSIR
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 mu g 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 mu g 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.
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