CELL-PROLIFERATION, DNA-REPAIR, AND P53 FUNCTION ARE NOT REQUIRED FOR PROGRAMMED DEATH OF PROSTATIC GLANDULAR CELLS INDUCED BY ANDROGEN ABLATION
CELL-PROLIFERATION, DNA-REPAIR, AND P53 FUNCTION ARE NOT REQUIRED FOR PROGRAMMED DEATH OF PROSTATIC GLANDULAR CELLS INDUCED BY ANDROGEN ABLATION
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DOI：
10.1073/pnas.90.19.8910
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发表时间：
1993-10-01
影响因子：
11.1
通讯作者：
ISAACS, JT
中科院分区：
文献类型：
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作者：
BERGES, RR;FURUYA, Y;ISAACS, JT
雄激素消融诱导雄激素依赖性前列腺腺细胞的程序性死亡，导致其基因组DNA片段化和细胞本身进入凋亡小体。在去势后第2 - 5天，每天有20%的前列腺细胞发生程序性死亡。在同一时期，95%的人死于G 0。在这些G 0腺细胞的程序性死亡期间，继DNA片段化之后诱导了无效的DNA修复过程。然而，这种无效的DNA修复不是必需的，因为用适当定时的羟基脲给药方案抑制该过程>90%对去势后这些细胞的程序性死亡的程度没有影响。同样，p53基因表达是不需要的，因为相同程度的细胞死亡发生在前列腺和精囊后，阉割野生型和p53缺陷型小鼠。
Androgen ablation induces programmed death of androgen-dependent prostatic glandular cells, resulting in fragmentation of their genomic DNA and the cells themselves into apoptotic bodies. Twenty percent of prostatic glandular cells undergo programmed death per day between day 2 and 5 after castration. During this same period, 95% of these die in G0. During the programmed death of these G0 glandular cells, a futile DNA repair process is induced secondary to the DNA fragmentation. This futile DNA repair is not required, however, since inhibition of this process by >90% with an appropriately timed hydroxy-urea dosing regimen had no effect upon the extent of the programmed death of these cells after castration. Likewise, p53 gene expression is not required since the same degree of cell death occurred in prostates and seminal vesicles after castration of wild-type and p53-deficient mice.