Significant inhibition of proliferative activity in PC3 human prostate cancer cells by estradiol is reported, accompanied by experimental evidence for a specific estrogen receptor (ER). Radioligand-binding assays revealed the presence of high affinity sites of estrogen binding in the nuclear compartment of PC3 cells. In addition, using a reverse transcriptase-polymerase chain reaction system, we obtained evidence of either normal or a variant ER mRNA; the latter, which lacks the entire exon 4, is coexpressed with normal ER mRNA and has been recently characterized in our laboratories. The likelihood that the inhibitory effect exerted by estradiol could be mediated by an increase of transforming growth factor β (TGFβ) production was also investigated. Use of monoclonal antibodies against TGFβ1 produced a 3-fold increase of growth rate in PC3 cells; this clearly speaks for high levels of endogenous TGFβ1. This effect was almost completely abolished after addition of 100 nm estradiol. However, we failed to demonstrate any increase of TGFβ1 mRNA after estradiol administration using Northern blot analysis. Further studies are needed to ascertain whether the estradiol-induced growth inhibition of PC3 cells is either mediated by other TGFβ species or exerted via alternative mechanism(s).


Partly supported by the Associazione Italiana per la Ricerca sul Cancro (AIRC) and the Consiglio Nazionale delle Ricerche, Special Project “Aging” (c.n. 93.435.PF40).

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