OVEREXPRESSION OF GML PROMOTES RADIATION-INDUCED CELL-CYCLE ARREST AND APOPTOSIS

Citation
K. Kagawa et al., OVEREXPRESSION OF GML PROMOTES RADIATION-INDUCED CELL-CYCLE ARREST AND APOPTOSIS, Biochemical and biophysical research communications, 241(2), 1997, pp. 481-485
Citations number
11
ISSN journal
0006291X
Volume
241
Issue
2
Year of publication
1997
Pages
481 - 485
Database
ISI
SICI code
0006-291X(1997)241:2<481:OOGPRC>2.0.ZU;2-Y
Abstract
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 sensitivi ty of cancer cells to ionizing radiation treatment, we established cel l 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 r adiation, whereas cells not expressing GML were resistant to irradiati on. Further investigation demonstrated that GML expression enhances G2 /M arrest and apoptosis induced by gamma-irradiation. These results su ggest that GML sensitizes cancer cells to ionizing radiation. (C) 1997 Academic Press.