Transfected c-myc and c-Ha-ras modulate radiation-induced apoptosis in rat embryo cells.
We studied radiation-induced apoptosis in rat embryo cells (REC) and in REC transfected with a c-myc oncogene [REC:myc(ch1)] or with a c-Ha-ras oncogene [REC:ras(ch1)], or both [REC:myc+ras(ch1)]. Apoptosis, evaluated in terms of altered morphology, dye exclusion and DNA fragmentation, was evident in all the irradiated cells. The development of apoptosis with time was initially rapid and then gradually saturated at > 36 h after irradiation. Radiation-induced apoptosis in REC:ras(ch1) was mildly reduced, but that in REC:myc(ch1) and REC:myc+ras(ch1) was significantly increased, relative to that in REC. The percentage of REC:myc(ch1) and REC:myc+ras(ch1) cells undergoing apoptosis increased rapidly at low doses to about 40% at 5 Gy irradiation and reached a plateau at high doses (of about 60% at > 15 Gy). In contrast, REC and REC:ras(ch1) were much less responsive, with a maximum of about 15 and 7%, respectively.
Chen
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CH
Laboratory of Radiation Biophysics, Memorial Sloan Kettering Cancer Center, New York, New York 10021.
Zhang
J
J
Ling
C C
CC
D000818:Animals; D017209:Apoptosis / Q000528:radiation effects; D001483:Base Sequence; D002478:Cells, Cultured; D004249:DNA Damage; D017931:DNA Primers / Q000737:chemistry; D004307:Dose-Response Relationship, Radiation; D005720:Gamma Rays; D016259:Genes, myc; D011905:Genes, ras; D008969:Molecular Sequence Data; D051381:Rats; D014162:Transfection
D017931:DNA Primers