Ruffion Alain, Al-Sakkaf Kaltoom A, Brown Barry L, Eaton Colby L, Hamdy Freddie C, Dobson Pauline R M
Department of Urology, Hopital Jules Courmont, Chemin du Grand Revoyet, 69495 Pierre Bénite Cedex, France.
Eur Urol. 2003 Mar;43(3):301-8. doi: 10.1016/s0302-2838(03)00038-1.
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.
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.
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.
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.
近期研究表明，人前列腺内存在涉及催乳素（PRL）的旁分泌/自分泌环。本研究旨在确定PRL对前列腺癌细胞生长和存活的影响以及这种影响背后的细胞内信号传导机制。
通过库尔特计数法评估PRL对LNCaP、PC3和DU145细胞增殖的影响。通过延时显微镜和膜联蛋白V结合法评估PRL对TRAIL、星形孢菌素和黄酮哌啶醇诱导的细胞凋亡的影响。通过蛋白质印迹法评估PRL受体（PRL-R）的状态和Akt/蛋白激酶B（PKB）的活性。
所有三种细胞系均表达PRL受体的短型和长型。虽然未发现PRL对这些细胞的增殖有显著影响，但PRL部分抑制了PC3细胞中TRAIL诱导的细胞凋亡。PRL还增强了这些细胞中Akt/PKB的磷酸化。
PRL对PC3、DU145和LNCaP的增殖无显著影响，但可能通过增强PC3细胞中Akt/PKB的磷酸化来抑制PC3细胞中TRAIL诱导的细胞凋亡。目前正在进行进一步研究，以确定PRL对其他两种前列腺癌细胞系的存活作用。
