Prostate cancer: a model of integration of genomic and non-genomic effects of the androgen receptor in cell lines model (Articolo in rivista)

Type
Label
  • Prostate cancer: a model of integration of genomic and non-genomic effects of the androgen receptor in cell lines model (Articolo in rivista) (literal)
Anno
  • 2008-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/j.steroids.2008.01.028 (literal)
Alternative label
  • Lorella Bonaccorsi; Daniele Nosi; Franco Quercioli; Lucia Formigli; Sandra Zecchi; Mario Maggi; Gianni Forti; Elisabetta Baldi (2008)
    Prostate cancer: a model of integration of genomic and non-genomic effects of the androgen receptor in cell lines model
    in Steroids
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Lorella Bonaccorsi; Daniele Nosi; Franco Quercioli; Lucia Formigli; Sandra Zecchi; Mario Maggi; Gianni Forti; Elisabetta Baldi (literal)
Pagina inizio
  • 1030 (literal)
Pagina fine
  • 1037 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 73 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
  • fasc. (9-10). Rapid Responses to Steroid Hormones. Elsevier. (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
  • 8 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Department of Clinical Physiopathology, Andrology Unit, Viale Pieraccini 6, I-50139 Florence, Italy Department of Anatomy, Histology & Forensic Medicine, University of Florence, Italy Institute for Complex Systems, National Research Council, Sesto Fiorentino, Firenze, Italy (literal)
Titolo
  • Prostate cancer: a model of integration of genomic and non-genomic effects of the androgen receptor in cell lines model (literal)
Abstract
  • Androgens and the androgen receptor (AR) are involved both in early tumorigenesis of prostate cancer (PCa) and in androgen-refractory disease. The role of AR signalling has also been highlighted by the fusion gene TMPRSS2:ERG recently identified in the majority of PCa. Several data indicate that re-expression of AR in PCa cell lines confers a less aggressive phenotype. We observed that re-expression of AR in the AR-negative cells PC3 decreases anchorage-independent growth and Matrigel invasiveness of PC3-AR cells where plasma membrane interaction between AR and EGFR led to an interference with downstream signalling and internalization of activated EGFR. Our data evidenced a shift of EGFR internalization pathway from the clathrin-coated pit one mediating signalling and recycling of EGFR to the lipid raft-mediated one mainly involved in lysosomal degradation of EGFR. These effects involved an altered recruitment to EGFR of the adaptor proteins Grb2 and c-Cbl followed by a reduced ubiquitination of EGFR. Our preliminary results suggest that in PC3-AR cells a pool of classical AR is located within cholesterol-rich membrane microdomains (namely as lipid rafts) and a population of EGFR is within cholesterol-rich membrane microdomains too. However, AR and EGFR membrane interaction that is increased by rapid androgen signalling is not within cholesterol-rich membrane microdomains. Our data enlighten that the crosstalk between genotropic and non-genotropic AR signalling interferes with signalling of EGFR in response to ligand leading to a lower invasive phenotype of AR-positive PCa cells. (literal)
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