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Carcinogenesis Advance Access published online on November 18, 2004
Carcinogenesis, doi:10.1093/carcin/bgh334
© 2004 by Oxford University Press
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Received May 4, 2004
Revised October 20, 2004
Accepted November 5, 2004

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

The signal transduction networks required for phosphorylation of STAT1 at Ser727 in mouse epidermal JB6 cells in the UVB response and inhibitory mechanisms of tea polyphenols

Tatyana A. Zykova 1, Yiguo Zhang 2, Feng Zhu 1, Ann M. Bode 1, and Zigang Dong 1*

1 Hormel Institute, University of Minnesota, Austin, Minnesota 55912, USA
2 Hormel Institute, University of Minnesota, Austin, Minnesota 55912, USA; University of Dundee, The Biomedical Research Centre, Level 5, Ninewells Hospital & Medical School, Dundee DD1 9SY, Scotland, United Kingdom

* To whom correspondence should be addressed.
Zigang Dong, E-mail: zgdong{at}hi.umn.edu


  Abstract

Signal Transducers and Activators of Transcription (STATs) play a critical role in signal transduction pathways. STATs are a family of cytoplasmic proteins with roles as signal messengers and transcription factors that participate in normal cellular responses to cytokines and growth factors. Phosphorylation of STAT1 at Ser727 is essential for its activation and occurs in response to stress signals, inflammation or infection. We observed that UVB induced phosphorylation of STAT1 (Ser727) in mouse epidermal JB6 Cl41 cells. This stimulation was inhibited by PD98059 and UO126, wortmannin or LY294002, SB202190 and SP600125, or a dominant negative mutant of ERK2 (DNM-ERK2), p38 (DNM-p38), or JNK1 (DNM-JNK1). The response was absent in Jnk1-/- or Jnk2-/- knockout cells, but was unaffected by a dominant negative mutant of the phosphatidylinositol-3 kinase (PI-3K) p85 subunit (DNM-{Delta}p85). STAT1 (Ser727) phosphorylation was also blocked in the Rsk2- cell line. In Pdk1-/- cells, STAT1 was not activated by UVB stimulation compared to a strong activation in Pdk1+/+ cells. Our data indicate that phosphorylation of STAT1 (Ser727) occurs through PI-3K, ERKs, p38 kinase, JNKs, PDK1, and p90RSK in the cellular response to UVB. We also show the inhibitory effect of theaflavins and EGCG on UVB-induced STAT1 (Ser727), ERKs, JNKs, PDK1 and p90RSK2 phosphorylation.


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