张珊文,肖卫群,吕有勇.照射后不同p53基因状态胃癌细胞的G1期阻滞和凋亡[J].中华放射医学与防护杂志,1999,19(5):322-324
照射后不同p53基因状态胃癌细胞的G1期阻滞和凋亡
G1 arrest and apoptosis of BGC 823 cell lines with different p53 status after irradiation
投稿时间:1998-06-07  修订日期:1998-11-22
DOI:
中文关键词:  抑癌基因p53  凋亡  辐射
英文关键词:Tumor suppressor gene p53  Apoptosis  Irradiation
基金项目:国家自然科学基金
作者单位
张珊文 100036 北京医科大学临床肿瘤学院放疗科 
肖卫群 100036 北京医科大学临床肿瘤学院放疗科 
吕有勇 北京市肿瘤分子生物学实验室 
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中文摘要:
      目的 评价抑癌基因p53(野生型p53)对照射后人胃癌细胞系(BGC823)的G1期阻滞和凋亡的控制作用。方法 3种具有不同p53状态的人胃癌细胞系,即转染人野生型p53基因的BGC-823-wtp53细胞、转染人突变型p53基因的BGC-823-mutp53细胞和转染无p53基因的空载质粒的BGC-823-vect细胞,用流式细胞计分析细胞,4Gy照射后0、8和24小时后各细胞时相分布和凋亡的反应。结果 照射4Gy后8小时和24小时后的BGC-823-wtp53细胞出现强烈的G1期阻滞(分别占原细胞总数的67.9%和61.1%),而BGC-823mutp53、BGC-823-vect细胞几乎没有G1期阻滞;照射4Gy后8小时和24小时后的BGC-823-wtp53细胞出现明显的预示凋亡的亚G1峰,凋亡细胞比例分别达13.0%和15.3%;而BGC-823-mutp53和BGC-823-vect细胞几乎没有出现亚G1峰和凋亡细胞比例都为零。结论 野生型p53基因具有促进照射后肿瘤细胞的G1期阻滞和凋亡作用,而p53变异和缺失则减低了肿瘤细胞对放射线的反应。
英文摘要:
      Objective To assess the role of the p53 tumor suppressor gene(wild-type p53) in G1 arrest and apoptosis after irradiation in human gastric carcinoma 823-cell lines(BGC823). Methods Three human gastric carcinoma 823-cell lines with different p53 status, i.e.BGC823-wtp53 cells with wild-type p53, BGC823-mutp53 cell with mutant p53 alleles and BGC823-vect without p53 gene, were used.Various cell phase distribution and apoptosis were analyzed by flow cytometry in 0, 8 and 24h following irradiation with 4Gy. Results The BGC823 wtp53 cells had strong arrest in G 1 phase at 8 and 24h following radiation with 4Gy (67 9% and 61 1% of original population, respectively), while the BGC823-mutp53 and BGC823-vect cells had almost no arrest in G 1 phase at 8 and 24h following radiation with 4Gy.In the BGC823-wtp53 cells, a sub G 1 phase peak of apoptosis could be observed at 8 and 24h after irradiation with 4Gy, apoptotic cell rates being 13 0% and 15 3%, respectively, while the BGC823-mutp53 and BGC823-vect cells had no apoptotic response after irradiation with 4Gy. Conclusion Wild type p53 genes promote G 1 phase arrest and apoptosis of tumor cells following irradiation, while those with mutant or vect p53 genes abrogate this response to irradiation.
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