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Endocrine-Related Cancer 11 (3) 537 -551     DOI: 10.1677/erc.1.00800
Copyright © 2004 by the Society for Endocrinology
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Loss of ERß expression as a common step in estrogen-dependent tumor progression

A Bardin1, N Boulle1,2, G Lazennec1, F Vignon1 and P Pujol1,2

1 Unité INSERM 540, 60 rue de Navacelles, 34090 Montpellier, France
2 Laboratoire de Biologie Cellulaire, Centre Hospitalier Universitaire de Montpellier, Hôpital Arnaud de Villeneuve, 271, Av G. Giraud, 34295 Montpellier, France

(Requests for offprints should be addressed to P Pujol, Service de Biologie Cellulaire, Hôpital Arnaud de Villeneuve, CHU, 271, Av G. Giraud, 34295 Montpellier, France; Email: p-pujol{at}chu-montpellier.fr)

The characterization of estrogen receptor beta (ERß) brought new insight into the mechanisms underlying estrogen signaling. Estrogen induction of cell proliferation is a crucial step in carcinogenesis of gynecologic target tissues, and the mitogenic effects of estrogen in these tissues (such as breast, endometrium and ovary) are well documented both in vitro and in vivo. There is also an emerging body of evidence that colon and prostate cancer growth is influenced by estrogens. In all of these tissues, most studies have shown decreased ERß expression in cancer as compared with benign tumors or normal tissues, whereas ER{alpha} expression persists. The loss of ERß expression in cancer cells could reflect tumor cell dedifferentiation but may also represent a critical stage in estrogen-dependent tumor progression. Modulation of the expression of ER{alpha} target genes by ERß or ERß-specific gene induction could explain that ERß has a differential effect on proliferation as compared with ER{alpha}. ERß may exert a protective effect and thus constitute a new target for hormone therapy, such as ligand specific activation. The potential distinct roles of ER{alpha} and ERß expression in carcinogenesis, as suggested by experimental and clinical data, are discussed in this review.




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