Document Type
Article
Publication Date
2014
Keywords
Egr-1, GADD45α, Arsenic, MAP kinase, Elk-1
Digital Object Identifier (DOI)
https://doi.org/10.18632/oncotarget.1995
Abstract
Long-term exposure to arsenic, an environmental contaminant, leads to increased risks of cancers. In the present study, we investigated the sequential regulation of Elk-1 and Egr-1 on As3+-induced GADD45α, an effector of G2/M checkpoint. We found that As3+ transcriptionally induced both Elk-1 and Egr-1, and NF-κB binding site was necessary for As3+-induced Egr-1 promoter activity. However, specific inhibition of JNK, ERK, and Elk-1 inhibited Egr-1 induction. Furthermore, silencing of Egr-1 downregulated As3+-induced expression of GADD45α and ChIP assay confirmed the direct binding of Egr-1 to GADD45α promoter. Taken together, our data indicated that the increase of GADD45α in response to As3+ was mediated sequentially by Elk-1 and Egr-1.
Rights Information
This work is licensed under a Creative Commons Attribution 3.0 License.
Was this content written or created while at USF?
Yes
Citation / Publisher Attribution
Oncotarget, v. 5, issue 11, p. 3862-3870
Scholar Commons Citation
Shi, Qiwen; Sutariya, Vijaykumar; Bishayee, Anupam; and Bhatia, Deepak, "Sequential Activation of Elk-1/Egr-1/GADD45α by Arsenic" (2014). Pharmacy Faculty Publications. 86.
https://digitalcommons.usf.edu/pharm_facpub/86
