Prostaglandin E2 Induces Fibroblast Growth Factor 9 via EP3-Dependent Protein Kinase Cδ and Elk-1 Signaling

Pei-Chin Chuang, Pei‐Chin Chuang, H Sunny Sun, Tsung-Ming Chen, Shaw-Jenq Tsai, Shaw‐Jenq Tsai
Molecular and cellular biology · 2006 · vol. 26(22) , pp. 8281–8292 · doi:10.1128/mcb.00941-06 · PMID:16982695 · PMC1636777 · W2168569494
article OA: green CC0 ⤵ 21 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Prostaglandin E2 induces fibroblast growth factor 9 expression in endometriotic stromal cells through the EP3 receptor, protein kinase Cdelta, and Elk-1 signaling pathway.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated how prostaglandin E2 (PGE2) regulates fibroblast growth factor 9 (FGF-9) expression in primary human endometriotic stromal cells, using time-course PGE2 stimulation, pharmacologic inhibitors, and siRNA knockdown, along with promoter analyses and signaling assays. The key finding was that PGE2 induces FGF-9 transcription through an EP3 receptor–dependent pathway involving PKCδ activation, ERK1/2 phosphorylation, and the transcription factor Elk-1, with two specific Elk-1 binding sites in the human FGF-9 promoter identified as crucial; a caveat is that the mechanistic work is largely confined to in vitro primary cell signaling and transcriptional regulation rather than in vivo confirmation. The paper further links the downstream functional consequence by stating that the induced FGF-9 promotes endometriotic stromal cell proliferation. This paper is centrally about endometriosis — it identifies PGE2/EP3-driven PKCδ/ERK/Elk-1 signaling as a mechanism for inducing FGF-9 in endometriotic stromal cells, with FGF-9 reported to promote endometriotic stromal proliferation.

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Abstract

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.

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Condition tags

endometriosis

MeSH descriptors

Dinoprostone ets-Domain Protein Elk-1 Fibroblast Growth Factor 9 Protein Kinase C-delta Receptors, Prostaglandin E RNA, Messenger Signal Transduction Cell Proliferation Dinoprostone Endometrium Endometrium Endometrium ets-Domain Protein Elk-1 Female Fibroblast Growth Factor 9 Fibroblast Growth Factor 9 Humans Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinase 3 Models, Biological

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