Arsenic-induced NF kappa beta transactivation through Erks- and JNKs-dependent pathways in mouse epidermal JB6 cells

Citation
Cs. Huang et al., Arsenic-induced NF kappa beta transactivation through Erks- and JNKs-dependent pathways in mouse epidermal JB6 cells, MOL C BIOCH, 222(1-2), 2001, pp. 29-34
Citations number
37
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cell & Developmental Biology
Journal title
MOLECULAR AND CELLULAR BIOCHEMISTRY
ISSN journal
0300-8177 → ACNP
Volume
222
Issue
1-2
Year of publication
2001
Pages
29 - 34
Database
ISI
SICI code
0300-8177(200106)222:1-2<29:ANKBTT>2.0.ZU;2-O
Abstract
Tumor promoting effects of arsenic are believed to be associated with its t ransactivation activity on transcription factors, such as AP-1 and NF kappa B. However, the results from different groups studying the effects of arsen ic on NF kappaB activation are contradictory in different cell models. Sinc e arsenic is a strong skin carcinogen, we have investigated the activation of NF kappaB by arsenic in a mouse skin epidermal cell line, JB6 cells. Exp osure of cells to arsenite or arsenate led to NF kappaB transactivation in mouse epidermal JB6 NF kappaB-luciferase reporter stable transfectants, C14 1 NF kappaB mass(1). This induction of NF kappaB activity by arsenic was do se- and time-dependent. The transactivation of NF kappaB by arsenic appeare d to be through activation of Erks and JNKs pathways because increased NF k appaB activity by arsenic could be dramatically inhibited by either pre-tre atment of cells with PD98059 or overexpression of dominant negative JNK(1). That Erks activation is required for arsenic-induced NF kappaB transactiva tion was further supported by the findings that arsenic-induced NF kappaB t ransactivation was impaired in JB6 30.7b cells, which were deficient in Erk s.