INCREASED EXPRESSION OF CYCLIN B1 MESSENGER-RNA COINCIDES WITH DIMINISHED G(2)-PHASE ARREST IN IRRADIATED HELA-CELLS TREATED WITH STAUROSPORINE OR CAFFEINE

Citation
Ej. Bernhard et al., INCREASED EXPRESSION OF CYCLIN B1 MESSENGER-RNA COINCIDES WITH DIMINISHED G(2)-PHASE ARREST IN IRRADIATED HELA-CELLS TREATED WITH STAUROSPORINE OR CAFFEINE, Radiation research, 140(3), 1994, pp. 393-400
Citations number
33
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Radiology,Nuclear Medicine & Medical Imaging
Journal title
ISSN journal
0033-7587
Volume
140
Issue
3
Year of publication
1994
Pages
393 - 400
Database
ISI
SICI code
0033-7587(1994)140:3<393:IEOCBM>2.0.ZU;2-B
Abstract
The irradiation of cells results in delayed progression through the G( 2) phase of the cell cycle. Treatment of irradiated HeLa cells with ca ffeine greatly reduces the G(2)-phase delay, while caffeine does not a lter progression of cells through the cell cycle in unirradiated cells . In this report we demonstrate that treatment of HeLa cells with the kinase inhibitor staurosporine, but not with the inhibitor H7, also re sults in a reduction of the G(2)-phase arrest after irradiation. Cell cycle progression in unirradiated cells is unaffected by 4.4 nM (2 ng/ ml) staurosporine, which releases the radiation-induced G(2)-phase arr est. In HeLa cells, the G(2)-phase delay after irradiation in S phase is accompanied by decreased expression of cyclin B1 mRNA. Coincident w ith the reduction in G(2)-phase delay, we observed an increase in cycl in B1 mRNA accumulation in irradiated, staurosporine-treated cells com pared to cells treated with irradiation alone. Caffeine treatment of i rradiated HeLa cells also resulted in an elevation in the levels of cy clin B1 message. These results support the hypothesis that diminished cyclin B1 mRNA levels influence G(2)-phase arrest to some degree. The findings that both staurosporine and caffeine treatments reverse the d epression in cyclin B1 expression suggest that these two compounds may act on a common pathway of cell cycle control in response to radiatio n injury.