OBJECTIVES: Recent studies suggest a paracrine/autocrine loop involving prolactin (PRL) within the human prostate. The aims of this study were to determine the effects of PRL on the growth and survival of prostate cancer cells and the intracellular signalling mechanisms underlying such effects. METHODS: The effect of PRL on proliferation of LNCaP, PC3 and DU145 was assessed by Coulter counting. The effect of PRL on TRAIL-, staurosporine- and flavopiridol-induced apoptosis was assessed by Timelapse microscopy and Annexin V binding. The status of the PRL receptor (PRL-R) and Akt/PKB (protein kinase B) activity were assessed by Western blotting. RESULTS: All three cell lines expressed both the short and long forms of the PRL receptor. Although, no significant effect of PRL on the proliferation of these cells was found, PRL partially inhibited TRAIL-induced apoptosis in PC3 cells. PRL also enhanced the phosphorylation of Akt/PKB in these cells. CONCLUSIONS: PRL had no significant effect on the proliferation of PC3, DU145 and LNCaP, but inhibited TRAIL-induced apoptosis in PC3 cells, possibly via enhanced Akt/PKB phosphorylation in PC3 cells. Further investigations are underway to determine the survival effect of PRL on the other two prostate cancer cell line. Copyright 2003 Elsevier Science B.V.
OBJECTIVES: Recent studies suggest a paracrine/autocrine loop involving prolactin (PRL) within the human prostate. The aims of this study were to determine the effects of PRL on the growth and survival of prostate cancer cells and the intracellular signalling mechanisms underlying such effects. METHODS: The effect of PRL on proliferation of LNCaP, PC3 and DU145 was assessed by Coulter counting. The effect of PRL on TRAIL-, staurosporine- and flavopiridol-induced apoptosis was assessed by Timelapse microscopy and Annexin V binding. The status of the PRL receptor (PRL-R) and Akt/PKB (protein kinase B) activity were assessed by Western blotting. RESULTS: All three cell lines expressed both the short and long forms of the PRL receptor. Although, no significant effect of PRL on the proliferation of these cells was found, PRL partially inhibited TRAIL-induced apoptosis in PC3 cells. PRL also enhanced the phosphorylation of Akt/PKB in these cells. CONCLUSIONS:PRL had no significant effect on the proliferation of PC3, DU145 and LNCaP, but inhibited TRAIL-induced apoptosis in PC3 cells, possibly via enhanced Akt/PKB phosphorylation in PC3 cells. Further investigations are underway to determine the survival effect of PRL on the other two prostate cancer cell line. Copyright 2003 Elsevier Science B.V.
Authors: D Giuffrida; A Perdichizzi; M C Giuffrida; S La Vignera; R D'Agata; E Vicari; A E Calogero Journal: J Endocrinol Invest Date: 2009-12-04 Impact factor: 4.256
Authors: Arunangshu Das; James D Bortner; Cesar A Aliaga; Aaron Baker; Anne Stanley; Bruce A Stanley; Matthew Kaag; John P Richie; Karam El-Bayoumy Journal: Prostate Date: 2012-08-21 Impact factor: 4.104
Authors: Naveen K Neradugomma; Dharmalingam Subramaniam; Ossama W Tawfik; Vincent Goffin; T Rajendra Kumar; Roy A Jensen; Shrikant Anant Journal: Carcinogenesis Date: 2013-11-21 Impact factor: 4.944
Authors: Sacha J Howell; Elizabeth Anderson; Tom Hunter; Gillian Farnie; Robert B Clarke Journal: Breast Cancer Res Date: 2008-08-05 Impact factor: 6.466