Gd. Kao et al., CYCLIN B1 AVAILABILITY IS A RATE-LIMITING COMPONENT OF THE RADIATION-INDUCED G(2) DELAY IN HELA-CELLS, Cancer research, 57(4), 1997, pp. 753-758
Irradiation of tumor cells results in a G(2) delay, which has been pos
tulated to allow DNA repair and cell survival, The G(2) delay after ir
radiation is marked in HeLa and other cells by delayed expression of c
yclin B1. To test whether this depression of cyclin B1 contributes to
the G(2) delay, we induced cyclin B1 expression in irradiated HeLa cel
ls using a dexamethasone-inducible promoter, Induction of cyclin B1 af
ter radiation abrogated the G(2) delay by approximately doubling the r
ate at which the cells reentered mitosis, whereas dexamethasone itself
had no effect, However, overexpression of cyclin B1 did not eliminate
the G(2) delay in irradiated cells. In unirradiated cells, overexpres
sion of cyclin B1 had no effect on cell cycle progression. Confirmatio
n that reduction of cyctin B1 levels would prolong G(2) was provided u
sing antisense oligonucleotides to cyclin B1. These results demonstrat
e that cyclin B1 levels control the length of the G(2) delay following
irradiation in HeLa cells but do not exclude additional mechanisms co
ntrolling the mitotic delay after irradiation.