| Literature DB >> 25639670 |
Sourav Chattopadhyay1, Sandeep Kumar Dash, Satyajit Tripathy, Balaram Das, Santanu Kar Mahapatra, Panchanan Pramanik, Somenath Roy.
Abstract
The purpose of this study was to determine the intracellular signaling transduction pathways involved in oxidative stress induced by nanoparticles in cancer cells. Activation of reactive oxygen species (ROS) has some therapeutic benefits in arresting the growth of cancer cells. Cobalt oxide nanoparticles (CoO NPs) are an interesting compound for oxidative cancer therapy. Our results showed that CoO NPs elicited a significant (P <0.05) amount of ROS in cancer cells. Co-treatment with N-aceyltine cystine (an inhibitor of ROS) had a protective role in cancer cell death induced by CoO NPs. In cultured cells, the elevated level of tumor necrosis factor-alpha (TNF-α) was noted after CoO NPs treatment. This TNF-α persuaded activation of caspase-8 followed by phosphorylation of p38 mitogen-activated protein kinase and induced cell death. This study showed that CoO NPs induced oxidative stress and activated the signaling pathway of TNF-α-Caspase-8-p38-Caspase-3 to cancer cells.Entities:
Keywords: ROS; TNF-α; cancer; cobalt oxide nanoparticles; p38-MAPK
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Year: 2015 PMID: 25639670 DOI: 10.1002/jat.3080
Source DB: PubMed Journal: J Appl Toxicol ISSN: 0260-437X Impact factor: 3.446