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Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells
Journal article   Open access   Peer reviewed

Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells

Fiorenza Ianzini, Alessandro Bertoldo, Elizabeth A Kosmacek, Stacia L Phillips and Michael A Mackey
Cancer cell international, Vol.6(1), pp.11-11
04/26/2006
DOI: 10.1186/1475-2867-6-11
PMCID: PMC1479380
PMID: 16640786
url
https://doi.org/10.1186/1475-2867-6-11View
Published (Version of record) Open Access

Abstract

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 lower 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 B1 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.
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