## Abstract Tumor suppressor p53 is an essential regulator in mammalian cellular responses to DNA damage including cell cycle arrest and apoptosis. Our study with Chinese hamster ovary CHO‐K1 cells indicates that when p53 expression and its transactivation capacity was inhibited by siRNA, UVC‐induc
Arrest of chinese hamster cells in G2 following treatment with the anti-tumor drug bleomycin
✍ Scribed by Robert A. Tobey
- Publisher
- John Wiley and Sons
- Year
- 1972
- Tongue
- English
- Weight
- 505 KB
- Volume
- 79
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Upon addition of bleomycin (BLM) to suspension cultures of Chinese hamster cells (line CHO), cells closer to prophase than 56 minutes continue dividing at the normal rate, whereas cells at earlier positions in the cell cycle either fail to reach mitosis altogether (at 200 pglml) or enter mitosis and divide at a reduced rate at lower drug concentrations. At 100 pglml of BLM (the rate of cell division slowed to a doubling time of 167 hours), initiation and termination of IjNA synthesis occur at normal rates, resulting in an accumulation of cells with a GP IjNA content in the first 130 minutes of Gz.
Bleomycin effects are not readily reversible. The rates of incorporation of leucine, uridine, or thymidine into cells treated for six hours with 100 pglml of BLM were 90, 85, and 8 0 % , respectively, of the values obtained in control cultures, suggesting that the effects of BLM on cell-cycle traverse cannot be correlated with gross inhibition of macromolecular synthesis.
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