Overexpression of GML promotes radiation-induced cell cycle arrest and apoptosis

被引:21
作者
Kagawa, K
Inoue, T
Tokino, T
Nakamura, Y
Akiyama, T
机构
[1] Osaka Univ, Res Inst Microbial Dis, Dept Oncogene Res, Osaka 565, Japan
[2] Osaka Univ, Sch Med, Dept Radiat Oncol, Osaka 565, Japan
[3] Univ Tokyo, Inst Med Sci, Mol Med Lab, Minato Ku, Tokyo 108, Japan
关键词
D O I
10.1006/bbrc.1997.7818
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Expression of the GML gene is regulated in a p53-dependent manner and is correlated with the sensitivity of esophageal cancer cells to anti-cancer drugs. To clarify the effect of GML expression on the sensitivity of cancer cells to ionizing radiation treatment, we established cell lines derived from p53-mutant human osteosarcoma HOS and esophageal carcinoma TE10 lines in which GML expression can be induced using the tetracycline-regulable system. Colony formation assay showed that the growth of cells expressing GML are inhibited in response to ionizing radiation, whereas cells not expressing GML were resistant to irradiation. Further investigation demonstrated that GML expression enhances G2/M arrest and apoptosis induced by gamma-irradiation. These results suggest that GML sensitizes cancer cells to ionizing radiation. (C) 1997 Academic Press.
引用
收藏
页码:481 / 485
页数:5
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