Does prolactin induce apoptosis? Evidences in a prostate cancer in vitro model

Abstract

Background: Prolactin (PRL) regulates prostate growth and differentiation. Some studies have suggested that PRL has a pro-apoptotic effect on a myeloma cell line and in newt spermatogonia. The proliferative effect of PRL on prostate cancer cell lines is, however, a controversial area.

Aim: On this account, we evaluated the effects of PRL on the prostate cancer cell lines LNCaP and PC3 apoptosis and proliferation.

Materials and methods: LNCaP and PC3 cells were exposed to increasing concentrations of PRL for 24, 48, 72 and 96 hours. Staining with propidium iodide (PI) and TUNEL assay followed by flow cytometry were used to detect apoptosis. LNCaP and PC3 proliferation was assessed by optical microscopy counting.

Results: PRL induced a dose-dependent decrease of DNA content and an increase of DNA fragmentation in LNCaP after 96 hours of incubation. These effects were observed with physiological concentrations of PRL and were counteracted by a prolactin receptor antagonist. On the other hand, PRL did not have any effect on DNA content or fragmentation in PC3 cells. No effect of PRL on LNCaP and PC3 proliferation was found.

Conclusions: This study indicates that PRL induces apoptosis in the androgen-responsive cell line LNCaP, whereas no effect was observed in the androgen-insensitive PC3 cell line. These findings suggest that androgen responsiveness may be required for PRL to be effective on prostatic cells.