Abstract
Tumor promoting effects of arsenic are believed to be associated with its transactivation activity on transcription factors, such as AP-1 and NFκB. However, the results from different groups studying the effects of arsenic on NFκB activation are contradictory in different cell models. Since arsenic is a strong skin carcinogen, we have investigated the activation of NFκB by arsenic in a mouse skin epidermal cell line, JB6 cells. Exposure of cells to arsenite or arsenate led to NFκB transactivation in mouse epidermal JB6 NFκB-luciferase reporter stable transfectants, C141 NFκB mass. This induction of NFκB activity by arsenic was dose- and time-dependent. The transactivation of NFκB by arsenic appeared to be through activation of Erks and JNKs pathways because increased NFκB activity by arsenic could be dramatically inhibited by either pre-treatment of cells with PD98059 or overexpression of dominant negative JNK1. That Erks activation is required for arsenic-induced NFκB transactivation was further supported by the findings that arsenic-induced NFκB transactivation was impaired in JB6 30.7b cells, which were deficient in Erks.
Original language | English |
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Pages (from-to) | 29-34 |
Number of pages | 6 |
Journal | Molecular and Cellular Biochemistry |
Volume | 222 |
Issue number | 1-2 |
DOIs | |
State | Published - 2001 |
Keywords
- Arsenic
- MAP kinase
- NFκB
ASJC Scopus subject areas
- Molecular Biology
- Clinical Biochemistry
- Cell Biology