Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Your Environment. Your Health.

Publication Detail

Title: Nickel compounds induce apoptosis in human bronchial epithelial Beas-2B cells by activation of c-Myc through ERK pathway.

Authors: Li, Qin; Suen, Ting-Chung; Sun, Hong; Arita, Adriana; Costa, Max

Published In Toxicol Appl Pharmacol, (2009 Mar 1)

Abstract: Nickel compounds are carcinogenic to humans and have been shown to alter epigenetic homeostasis. The c-Myc protein controls 15% of human genes and it has been shown that fluctuations of c-Myc protein alter global epigenetic marks. Therefore, the regulation of c-Myc by nickel ions in immortalized but not tumorigenic human bronchial epithelial Beas-2B cells was examined in this study. It was found that c-Myc protein expression was increased by nickel ions in non-tumorigenic Beas-2B and human keratinocyte HaCaT cells. The results also indicated that nickel ions induced apoptosis in Beas-2B cells. Knockout of c-Myc and its restoration in a rat cell system confirmed the essential role of c-Myc in nickel ion-induced apoptosis. Further studies in Beas-2B cells showed that nickel ion increased the c-Myc mRNA level and c-Myc promoter activity, but did not increase c-Myc mRNA and protein stability. Moreover, nickel ion upregulated c-Myc in Beas-2B cells through the MEK/ERK pathway. Collectively, the results demonstrate that c-Myc induction by nickel ions occurs via an ERK-dependent pathway and plays a crucial role in nickel-induced apoptosis in Beas-2B cells.

PubMed ID: 19135467 Exiting the NIEHS site

MeSH Terms: Apoptosis/drug effects*; Blotting, Western; Cell Line; Epithelial Cells/drug effects*; Extracellular Signal-Regulated MAP Kinases/physiology*; Flow Cytometry; Genes, Reporter; Humans; Keratinocytes/drug effects; Luciferases/metabolism; Nickel/toxicity*; Proto-Oncogene Proteins c-myc/physiology*; RNA/biosynthesis; RNA/genetics; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction/drug effects; ras Proteins/genetics; ras Proteins/physiology

Back
to Top