CYCLIN B1 AVAILABILITY IS A RATE-LIMITING COMPONENT OF THE RADIATION-INDUCED G(2) DELAY IN HELA-CELLS

Citation
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
Citations number
48
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Oncology
Journal title
ISSN journal
0008-5472
Volume
57
Issue
4
Year of publication
1997
Pages
753 - 758
Database
ISI
SICI code
0008-5472(1997)57:4<753:CBAIAR>2.0.ZU;2-N
Abstract
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.