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1: Mol Cell Biol. 2006 Nov;26(22):8281-92. Epub 2006 Sep 18.

Prostaglandin E2 induces fibroblast growth factor 9 via EP3-dependent protein
kinase Cdelta and Elk-1 signaling.

Chuang PC, Sun HS, Chen TM, Tsai SJ.

Institute of Basic Medical Sciences, National Cheng Kung University Medical
College, Tainan 701, Taiwan, Republic of China.

Fibroblast growth factor 9 (FGF-9) is a potent mitogen that controls the proper
development of many tissues and organs. In contrast, aberrant expression of FGF-9
also results in the evolution of many human diseases, such as cancers and
endometriosis. Despite its vital function being reported, the cellular and
molecular mechanisms responsible for the regulation of FGF-9 expression are
mostly unknown. We report here that prostaglandin E2 (PGE2) induces expression of
FGF-9, which promotes endometriotic stromal cell proliferation, through the EP3
receptor-activated protein kinase Cdelta (PKCdelta) signaling pathway. Activation
of PKCdelta leads to phosphorylation of ERK1/2, and the transcription factor
Elk-1 thereby promotes transcription of FGF-9. Two Elk-1 cis-binding sites
located at nucleotides -1324 to -1329 and -1046 to -1051 of the human FGF-9
promoter are identified as crucial for mediating PGE2 actions. Collectively, we
demonstrate, for the first time, that PGE2 can directly induce FGF-9 expression
via a novel signaling pathway involving EP3, PKCdelta, and a member of the ETS
domain-containing transcription factor superfamily in primary human endometriotic
stromal cells. Our findings may also provide a molecular framework for
considering roles for PGE2 in FGF-9-related embryonic development and/or human
diseases.

PMID: 16982695 [PubMed - indexed for MEDLINE]

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