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A more recent version of this article appeared on October 1, 2002
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Submitted on March 20, 2002
Revised on May 27, 2002
Accepted on July 16, 2002
1 Dipartimento di Biologia, Università "Roma Tre", V.le G. Marconi, 446, I-00146 Roma
2 Dipartimento di Patologia Generale, Seconda Università degli Studi di Napoli, Vico L. De Crecchio, 7, I-80138 Napoli, Italy
* Corresponding author. E-mail address: m.marino{at}uniroma3.it.
Estrogens induce cell proliferation in target tissues by stimulating progression through the G1 phase of the cell cycle. Activation of cyclin D1 gene expression is a critical feature of this hormonal action. The existence of rapid/non-genomic estradiol-regulated PKC-
and ERK signal transduction pathways, their cross-talk and role played in DNA synthesis and cyclin D1 gene transcription have been studied here in human hepatoma HepG2 cells. 17ß-estradiol was found to rapidly activate PKC- translocation and ERK-2/MAP kinase phosphorylation in this cell line. These actions were independent of each other, preceding the increase of thymidine incorporation into DNA and cyclin D1 expression, and did not involve DNA binding by estrogen receptor (ER). The results obtained with specific inhibitors indicated that PKC- pathway is necessary to mediate the estradiol-induced G1-S progression of HepG2 cells, but it does not exert any effect(s) on cyclin D1 gene expression. On the contrary, ERK-2 cascade was strongly involved in both G1-S progression and cyclin D1 gene transcription. Deletion of its Activating Protein-1 responsive element motif resulted in attenuation of cyclin D1 promoter responsiveness to estrogen. These results indicate that estrogen-induced cyclin D1 transcription can occur in HepG2 cells independently of the transcriptional activity of ER sustaining the pivotal role played by non genomic pathways of estrogen action in hormone-induced proliferation.
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