DELAYED CYCLIN B1 EXPRESSION DURING THE G2 ARREST FOLLOWING DNA-DAMAGE

Citation
A. Maity et al., DELAYED CYCLIN B1 EXPRESSION DURING THE G2 ARREST FOLLOWING DNA-DAMAGE, Oncogene, 13(8), 1996, pp. 1647-1657
Citations number
56
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Oncology,Biology,"Cell Biology
Journal title
ISSN journal
0950-9232
Volume
13
Issue
8
Year of publication
1996
Pages
1647 - 1657
Database
ISI
SICI code
0950-9232(1996)13:8<1647:DCBEDT>2.0.ZU;2-2
Abstract
Exposure of cells to DNA damaging agents results in a G2 arrest. Expos ure of HeLa cells to camptothecin, etoposide or nitrogen mustard for 1 h in S phase resulted in delayed expression of cyclin B1 mRNA during the G2 arrest. Initially the levels of cyclin B1 protein were low as w ell; however, with extended time the cells blocked in G2 regained high er levels of cyclin B1 protien. In the case of cells treated with nitr ogen mustard the higher levels coincided with cells exiting the G2 blo ck into G1. However, with camptothecin or etoposide treatment, while t he accumulation of cyclin B1 protein was delayed, its levels eventuall y surpassed peak levels seen in control cells, in spite of the fact th at cells were still blocked in G2. These cells did not continue to pro gress through the cell cycle indicating further complexity to the mech anisms underlying the G2 block. Decreased transcription and stability of cyclin B1 mRNA were shown to occur after treatment with these DNA d amaging agents. These results indicate that suppression of cyclin B1 m RNA expression is one consequence of DNA damage in HeLa cells.