Université de Caen, Laboratoire de biologie moléculaire et cellulaire de la signalisation, UPRES-EA 3919, IFR 146 ICORE, avenue côte de Nacre, 14032 Caen, France.
J Neuroimmunol. 2010 Mar 30;220(1-2):69-78. doi: 10.1016/j.jneuroim.2010.01.010. Epub 2010 Feb 16.
As opioid receptors modulate proliferation and apoptosis of immune cells, we hypothesized that they could reduce malignant haematopoietic cells. After screening, we selected the human multiple myeloma LP-1 cells which express mu- (MOP-) and kappa-opioid receptors (KOP-R). U50 488 produces a modest but significant decrease in viability associated with an arrest in the G0/G1 phase, but not antagonized by NorBNI and not associated with modulation of p21(Cip1), p27(Kip1) or p53 expression. In contrast, no effect was observed with dynorphin, U69 593 and morphine. In conclusion, the anti-proliferative effects of U50 488 are not mediated by KOP-R in the LP-1 cells.
由于阿片受体调节免疫细胞的增殖和凋亡，我们假设它们可以减少恶性造血细胞。经过筛选，我们选择表达μ-（MOP-）和κ-阿片受体（KOP-R）的人多发性骨髓瘤 LP-1 细胞。U50488 产生适度但显著的细胞活力降低，与 G0/G1 期阻滞相关，但不受 NorBNI 拮抗，与 p21(Cip1)、p27(Kip1)或 p53 表达的调节无关。相反，用 dynorphin、U69593 和吗啡则没有观察到效果。总之，U50488 在 LP-1 细胞中的抗增殖作用不是由 KOP-R 介导的。
