Marushige Y, Marushige K, Koestner A
Department of Pathology, Michigan State University, East Lansing 48824.
Anticancer Res. 1992 Nov-Dec;12(6B):2069-73.
Nerve growth factor (NGF) inhibited cellular DNA synthesis of rat T9 anaplastic glioma cells in a dose-dependent manner in the range of 0.5-5 micrograms/ml. Oxidation of 2 to 3 tryptophan residues of NGF, which had been known to destroy biological and immunological activity, greatly diminished its inhibitory effect on DNA synthesis. The inhibition was also abolished by anti-NGF IgG. Flow cytometric analyses and immunocytochemical assays of DNA synthesis using bromodeoxyuridine incorporation at various times during cell exposure to NGF revealed that the growth inhibition was attributable to gradual accumulation of growth-arrested cells at the G1 phase. Synthesis of nuclear regulatory proteins JUN and p53 was inhibited preferentially and progressively by NGF as inhibition of DNA synthesis increased.
神经生长因子（NGF）在0.5 - 5微克/毫升范围内以剂量依赖方式抑制大鼠T9间变性胶质瘤细胞的细胞DNA合成。已知破坏生物和免疫活性的NGF的2至3个色氨酸残基的氧化，大大减弱了其对DNA合成的抑制作用。抗NGF IgG也消除了这种抑制作用。在细胞暴露于NGF的不同时间使用溴脱氧尿苷掺入进行的DNA合成的流式细胞术分析和免疫细胞化学测定表明，生长抑制归因于生长停滞细胞在G1期的逐渐积累。随着DNA合成抑制的增加，核调节蛋白JUN和p53的合成被NGF优先且逐渐抑制。
