Cristofanon Silvia, Uguccioni Francesco, Cerella Claudia, Radogna Flavia, Dicato Mario, Ghibelli Lina, Diederich Marc
Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Fondation Recherche sur le Cancer et les Maladies du Sang, Hôpital Kirchberg, Luxembourg.
Ann N Y Acad Sci. 2009 Aug;1171:472-8. doi: 10.1111/j.1749-6632.2009.04896.x.
We have shown that melatonin exerts a prooxidant activity in U937 cells, a tumor human promonocytic cell line. (1) Here we show that melatonin induces a strong canonical activation of NF-kappaB, inducing IkappaBalpha degradation and the consequential nuclear translocation of p50/p65 subunits. The timing of NF-kappaB activation overlaps with the timing of reactive oxygen species (ROS) production due to melatonin. Overexpression of dominant-negative IkappaB, which prevents a possible NF-kappaB activation, transformed melatonin in a proapoptotic molecule. These data indicate for the first time that melatonin can trigger NF-kappaB activation and might suggest a possible role for ROS induced by melatonin. Results indicate a possible involvement in the survival pathway of melatonin-generated ROS as secondary messengers.
我们已经证明褪黑素在人肿瘤原单核细胞系U937细胞中发挥促氧化活性。（1）在此我们表明，褪黑素诱导NF-κB强烈的经典激活，诱导IκBα降解以及p50/p65亚基随后的核转位。NF-κB激活的时间与褪黑素诱导的活性氧（ROS）产生的时间重叠。显性负性IκB的过表达可防止可能的NF-κB激活，从而将褪黑素转变为促凋亡分子。这些数据首次表明褪黑素可触发NF-κB激活，并可能提示褪黑素诱导的ROS的潜在作用。结果表明褪黑素产生的ROS作为第二信使可能参与生存途径。
