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doi: 10.1038/onc.2010.380
pmid: 20802529
Cisplatin is a widely used cancer chemotherapeutic that promotes DNA damage-associated apoptosis. Although platinum compounds are known to form DNA adducts and provoke DNA damage, the molecular mechanism of cisplatin-induced cell death remains unclear. In this article, we show that the BH3-only protein Noxa is strongly transcriptionally upregulated in response to cisplatin and related platinum compounds. Cisplatin-induced Noxa expression was ERK dependent, but p53 independent, and inhibition of ERK activation markedly attenuated cisplatin-induced cell death, as well as Noxa expression. Furthermore, siRNA-mediated ablation of Noxa expression also inhibited cisplatin-induced cell death and permitted clonogenic survival. These observations reveal a novel ERK-regulated route to Noxa expression that is important for the cell killing activity of platinum-based chemotherapeutic drugs.
Leupeptins, Antineoplastic Agents, Apoptosis, Platinum Compounds, Up-Regulation, Proto-Oncogene Proteins c-bcl-2, Humans, Cisplatin, Tumor Suppressor Protein p53, Extracellular Signal-Regulated MAP Kinases, DNA Damage, HeLa Cells
Leupeptins, Antineoplastic Agents, Apoptosis, Platinum Compounds, Up-Regulation, Proto-Oncogene Proteins c-bcl-2, Humans, Cisplatin, Tumor Suppressor Protein p53, Extracellular Signal-Regulated MAP Kinases, DNA Damage, HeLa Cells
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 78 | |
popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |