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Endocrinology Vol. 141, No. 9 3172-3182
Copyright © 2000 by The Endocrine Society

ARTICLES

Androgen Receptor Expression in Prostate Carcinoma Cells Suppresses {alpha}6ß4 Integrin-Mediated Invasive Phenotype1

Lorella Bonaccorsi, Vinicio Carloni, Monica Muratori, Adriana Salvadori, Augusto Giannini, Marco Carini, Mario Serio, Gianni Forti and Elisabetta Baldi

Department of Clinical Physiopathology (L.B., M.M., G.F., E.B.), Andrology Unit (M.S.), Internal Medicine (V.C.) and Urology (M.C.), University of Florence, viale Pieraccini 6, I-50139 Florence, Italy; U.O. Anatomia Patologica Ospedale S. Maria Annunziata (A.S., A.G.), I-50139 Florence, Italy

Address all correspondence and requests for reprints to: Elisabetta Baldi, Department of Clinical Physiopathology, Andrology Unit, University of Florence, viale Pieraccini, 6, I-50139, Florence, Italy. E-mail: e.baldi{at}dfc.unifi.it

Prostate cancer cells may lose androgen-sensitivity after androgen ablation therapy, becoming highly invasive and metastatic. The biological mechanisms responsible for higher tumurogenicity of androgen-independent prostate carcinomas are not entirely known. We demonstrate that androgen receptor regulation of adhesion and invasion of prostate cancer cells through modulation of {alpha}6ß4 integrin expression may be one of the molecular mechanisms responsible of this phenomenon. We found that protein and gene expressions of {alpha}6 and ß4 subunits were strongly reduced in the androgen-sensitive cell line LNCaP respect to the androgen-independent PC3 and that transfection of PC3 cells with a full-length androgen receptor expression vector resulted in a decreased expression of {alpha}6ß4 integrin, reduced adhesion on laminin, and suppressed Matrigel invasion. Growth in soft agar was also suppressed in androgen receptor-positive PC3 clones. Treatment of androgen receptor positive clones with the synthetic androgen R1881 further reduced {alpha}6 and ß4 messenger RNA expression as well as adhesion on laminin and Matrigel invasion. Our results indicate that androgens regulate cell-extracellular matrix adhesion and invasion by modulation of integrin expression and function, thus keeping a low invasive phenotype of prostate cancer cells.




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