Aim: 

Prostate cancer represents the second leading cause of cancer-related death in men with no effective therapeutic management for metastatic disease. Estrogen are key signaling molecules that regulate various physiological and pathological processes, such as prostate cancer. Epidemiological and experimental studies suggest that estrogens may have both cancerogenic and chemiopreventive effects on the prostatic epithelium. These divergent effects may reflect the presence of two distinct receptors, the estrogen receptor alpha (ERa) and beta (ERb). ERb has been mainly implicated for the benefical effects of estrogens.

Methods: 

In the present study, we examined the function of ERb on the motility of the DU 145 human prostate cancer cell line. To activate the ERb receptor, the ERb–selective agonist diarylproprionitrile (DPN) has been used and 1) the intracellular localization of ERb receptor by immunofluorescence and Western blot experiments, 2) the migratory behaviour of the cells as well as 3) the integrin expression have been evaluated.

Results: 

The immunofluorescence studies suggest that ERb is localized in the cytoplasmic level and doesn't translocate to the nucleus after treatment with DPN; this observaton was confirmed by Western blot on nuclear and cytosolic fraction of the cells. The migratory assay shows that, after DPN treatment (1 or 24h), cell motility was significantly reduced. To evaluate if this fact might be due to changes in integrin expression, we analyzed the expression of av, a2, b1 and b4 integrins after DPN treatment ( 24, 48, 72 h). We observed that only av integrin expression was significantly reduced after a treatment of 24 h with DPN.

Conclusion: 

In summary, these data indicate that, in DU 145 cells: 1) ERb is mainly localized in the cytoplasm and does not translocate to the nucleus; 2) ERb activation modulates the migratory behaviour of the cells; 3) this anti-migratory effect might involve av subunit integrin.