J. Lipid Res.
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A more recent version of this article appeared on December 1, 2005

Papers In Press, published online ahead of print September 14, 2005
J. Lipid Res., doi:10.1194/jlr.M500154-JLR200
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Submitted on April 19, 2005
Revised on September 2, 2005
Accepted on September 8, 2005

KGF induces lipogenic genes through a PI3K and JNK/SREBP-1 pathway in H292 cells

Yongsheng Chang, Jieru Wang, Xiaojun Lu, Douglas P. Thewke, and Robert J. Mason

Medicine Dept., National Jewish Medical and Research Center, Denver, CO 80206

Corresponding Author: warrent{at}njc.org

Lipid synthesis is required for cell growth and is subject to pharmacologic regulation. Keratinocyte growth factor (KGF) stimulates proliferation and lipogenesis in H292 cells, a pulmonary epithelial cancer cell line, but the signaling pathways are not known. KGF stimulated the expression of the transcription factors, SREBP-1, C/EBPalpha , and C/EBPdelta , and two key enzymes involved in lipogenesis, fatty acid synthase (FAS) and stearoyl coenzyme A desaturase 1 (SCD-1). We found that KGF induced rapid activation of Akt, p70S6K, JNK, and ERK. Induction of SREBP-1, SCD-1, and FAS by KGF was inhibited by the JNK inhibitor SP600125 and the PI3 kinase inhibitor LY294002 but not by the ERK inhibitor PD98059. Using FAS and SCD-1-luciferase promoter constructs, we observed that KGF stimulated the transcription of these promoters and that exogenous cholesterol inhibited the induction. Mutation of the SREBP-1 binding site in the SCD-1 promoter abolished the effect of KGF on SCD-1 transcription. In addition, overexpression of active SREBP-1 directly stimulated SCD-1 and FAS. Conversely, adenovirus-mediated overexpression of a dominant negative of SREBP-1 inhibited the KGF effect on FAS and SCD-1 expression. In summary, we conclude that KGF requires both PI3 kinase and JNK signaling pathways to induce SREBP-1, which in turn induces SCD-1, and FAS expression in H292 cells.


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