Bracey T S, Miller J C, Preece A, Paraskeva C
Dept. of Pathology and Microbiology, School of Medical Sciences, University of Bristol, UK.
Oncogene. 1995 Jun 15;10(12):2391-6.
The tumour suppressor gene p53 codes for a transcription factor which is thought to play a critical role in the induction of G1 cell cycle arrest and programmed cell death (apoptosis) following DNA damage by ionizing radiation. The aim of this investigation was to determine whether a p53 independent radiation-induced apoptosis pathway exists in human colon epithelial cell lines. This report describes the induction, by gamma-radiation, of apoptosis in the colorectal adenoma cell line S/RG/C2, and in the colorectal carcinoma cell line PC/JW, both of which lack wild type p53. In addition, flow cytometry revealed that both cell lines failed to arrest in G1 after radiation. Thus, although loss of wild type p53 may abrogate G1 arrest, radiation-induced apoptosis can still occur in human colonic tumour cell lines through a p53 independent mechanism.
肿瘤抑制基因p53编码一种转录因子，该转录因子被认为在电离辐射导致DNA损伤后诱导G1期细胞周期停滞和程序性细胞死亡（凋亡）过程中发挥关键作用。本研究的目的是确定在人结肠上皮细胞系中是否存在一条不依赖p53的辐射诱导凋亡途径。本报告描述了γ辐射诱导大肠腺瘤细胞系S/RG/C2和大肠癌细胞系PC/JW发生凋亡的情况，这两种细胞系均缺乏野生型p53。此外，流式细胞术显示这两种细胞系在辐射后均未停滞在G1期。因此，尽管野生型p53的缺失可能消除G1期停滞，但辐射诱导的凋亡仍可通过不依赖p53的机制在人结肠肿瘤细胞系中发生。
