Background: We have demonstrated that in some human cancer cells both chronic mild heat and ionizing radiation exposures induce a transient block in S and G2 phases of the cell cycle. During this delay, cyclin B1 protein accumulates to supranormal levels, cyclin B1-dependent kinase is activated, and abrogation of the G2/M checkpoint control occurs resulting in mitotic catastrophe (MC). Results: Using syngenic mouse embryonic fibroblasts (MEF) with wild-type or mutant p53, we now show that, while both cell lines exhibit delays in S/G2 phase post-irradiation, the mutant p53 cells show elevated levels of cyclin B1 followed by MC, while the wild-type p53 cells present both a ower accumulation of cyclin B1 and a lower frequency of MC. Conclusion: These results are in line with studies reporting the role of p53 as a post-transcriptional regulator of cyclin BI protein and confirm that dysregulation of cyclin B1 promote radiation-induced MC. These findings might be exploited to design strategies to augment the yield of MC in tumor cells that are resistant to radiation-induced apoptosis. © 2006 Ianzini et al; licensee BioMed Central Ltd.
CITATION STYLE
Ianzini, F., Bertoldo, A., Kosmacek, E. A., Phillips, S. L., & Mackey, M. A. (2006). Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells. Cancer Cell International, 6. https://doi.org/10.1186/1475-2867-6-11
Mendeley helps you to discover research relevant for your work.