ATF2 is a subfamily member of AP-1 and has an important role in cellular stress responses.
ATF2 has been implicated in a transcriptional response leading to cell migration and malignant tumor progression. However, little is known about the effect of arsenic on expression of ATF2 and regulatory pathways in human urothelial cells. In this study, ATF2 expression was measured in NaAsO2-treated human uroepithelial cell line (SV-HUC-1) with 1, 2, 4, 8 and 10 μM concentrations in order to provide some basis data for the study on mechanism of bladder cancer induced by arsenic. We found that ATF2 expression levels at 2, 4, 8 and 10 μM arsenic-treated cells were significantly higher than those of control cells, and the strongest expression occurred in 4 μM NaAsO2-treated cells. Antioxidants (melatonin) and JNK or p38 inhibitors decreased significantly arsenic-induced ATF2 expression. Taken together, these data indicated that the increasing of ATF2 expression is mediated via oxidative stress induced by arsenic in SV-HUC-1 cells, and JNK or p38 rather than ERK is responsible for arsenic-induced ATF2 expression. ROS were also involved in arsenic induced the activation of JNK and p38 MAPK signaling pathway.
Written by:
Liu S, Wang F, Yan L, Zhang L, Song Y, Xi S, Jia J, Sun G. Are you the author?
Department of Environmental and Occupational Health, Liaoning Provincial Key Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health, China Medical University, District of Heping, North Er Road, No. 92, Shenyang City, 110001, China.
Reference: Arch Toxicol. 2013 Apr 17. Epub ahead of print.
doi: 10.1007/s00204-013-1058-9
PubMed Abstract
PMID: 23591579
UroToday.com Investigative Urology Section
