Duffey D C, Calcaterra T C, Lichtenstein A K
Division of Head and Neck Surgery, University of California at Los Angeles School of Medicine, 90024-1624, USA.
Laryngoscope. 1996 Jul;106(7):889-94. doi: 10.1097/00005537-199607000-00020.
The apoptotic cell death in Cal-27 cells induced by exposure to transforming growth factor-beta 1 was inhibited by the endonuclease inhibitor aurintricarboxylic acid (ATA) in a concentration-dependent fashion. In vitro studies of cytotoxicity, DNA fragmentation, and protein synthesis by Cal-27 cell lines were performed. Inhibition of cytotoxicity as well as endonucleolytic DNA cleavage was detected. ATA did not inhibit cytotoxicity either via transforming growth factor cell-surface-receptor alteration or by inhibition of macromolecular synthesis. ATA-sensitive events occurred late during treatment. These data suggest that endonucleolytic DNA cleavage is a mandatory event leading to cell death in this system.
在暴露于转化生长因子-β1 诱导的 Cal-27 细胞凋亡性细胞死亡,可被核酸内切酶抑制剂金精三羧酸(ATA)以浓度依赖的方式抑制。对 Cal-27 细胞系进行了细胞毒性、DNA 片段化和蛋白质合成的体外研究。检测到细胞毒性以及核酸内切酶介导的 DNA 裂解受到抑制。ATA 既不通过转化生长因子细胞表面受体改变也不通过抑制大分子合成来抑制细胞毒性。ATA 敏感事件发生在处理后期。这些数据表明核酸内切酶介导的 DNA 裂解是该系统中导致细胞死亡的必要事件。