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Papers In Press, published online ahead of print January 11, 2002
Environmental Health Sciences, Case Western Reserve University, School of Medicine, Cleveland, OH 44106
Corresponding Author: ear4{at}po.cwru.edu
Human papillomavirus (HPV) is an important etiological agent in the genesis of cervical cancer. HPV-positive cervical tumors and human papillomavirus-positive cell lines display increased epidermal growth factor receptor (EGFR) expression, which is associated with increased cell proliferation. ECE16-1 cells are an HPV-immortalized human ectocervical epithelial cell line that is a model of HPV-associated cervical neoplasia and displays elevated EGFR levels. In the present study, we evaluate the effects of receptor-selective retinoid ligands on EGFR-associated signal transduction. We show that retinoic acid receptor (RAR)-selective ligands reduce EGFR level, and the magnitude and duration of EGFR activation in EGF-stimulated cells. These effects are reversed by cotreatment with an RAR-antagonist. To identify the mechanism, we examined the effects of retinoid treatments on EGF-dependent signaling. Stimulation with EGF causes a biphasic activation of the ERK1/2 MAPK. The first peak of activation is present at 20 min and the second at 36 h. This activation subsequently leads to an increase in cyclin D1 level and increased cell proliferation. Simultaneous treatment with EGF and a retinoic acid receptor (RAR)-selective retinoid inhibits both phases of ERK1/2 activation, completely eliminates the cyclin D1 induction, and suppresses EGF dependent cell proliferation. This effect is specific, as retinoid treatment does not alter the level or activity of other EGFR-regulated kinases, including AKT and the MAPK’s p38 and JNK. Retinoid X receptor (RXR)-selective ligands, in contrast, did not regulate these responses. These results suggest that RAR ligand-associated down-regulation of EGFR activity reduces cell proliferation by reducing the magnitude and duration of EGF-dependent ERK1/2 activation.
J. Biol. Chem, 10.1074/jbc.M110897200
Submitted on November 13, 2001
Revised on January 7, 2002
Accepted on January 11, 2002
Retinoids suppress epidermal growth factor-associated cell proliferation by inhibiting epidermal growth factor receptor-dependent ERK1/2 activation
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