Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells
<p>Abstract</p> <p>Background</p> <p>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 supranorm...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2006-04-01
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| Series: | Cancer Cell International |
| Online Access: | http://www.cancerci.com/content/6/1/11 |
| _version_ | 1818145558197436416 |
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| author | Phillips Stacia L Kosmacek Elizabeth A Bertoldo Alessandro Ianzini Fiorenza Mackey Michael A |
| author_facet | Phillips Stacia L Kosmacek Elizabeth A Bertoldo Alessandro Ianzini Fiorenza Mackey Michael A |
| author_sort | Phillips Stacia L |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>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).</p> <p>Results</p> <p>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.</p> <p>Conclusion</p> <p>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.</p> |
| first_indexed | 2024-12-11T12:05:22Z |
| format | Article |
| id | doaj.art-88ed9c22ae20483185b71d7cac922f22 |
| institution | Directory Open Access Journal |
| issn | 1475-2867 |
| language | English |
| last_indexed | 2024-12-11T12:05:22Z |
| publishDate | 2006-04-01 |
| publisher | BMC |
| record_format | Article |
| series | Cancer Cell International |
| spelling | doaj.art-88ed9c22ae20483185b71d7cac922f222022-12-22T01:07:58ZengBMCCancer Cell International1475-28672006-04-01611110.1186/1475-2867-6-11Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cellsPhillips Stacia LKosmacek Elizabeth ABertoldo AlessandroIanzini FiorenzaMackey Michael A<p>Abstract</p> <p>Background</p> <p>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).</p> <p>Results</p> <p>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.</p> <p>Conclusion</p> <p>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.</p>http://www.cancerci.com/content/6/1/11 |
| spellingShingle | Phillips Stacia L Kosmacek Elizabeth A Bertoldo Alessandro Ianzini Fiorenza Mackey Michael A Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells Cancer Cell International |
| title | Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells |
| title_full | Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells |
| title_fullStr | Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells |
| title_full_unstemmed | Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells |
| title_short | Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells |
| title_sort | lack of p53 function promotes radiation induced mitotic catastrophe in mouse embryonic fibroblast cells |
| url | http://www.cancerci.com/content/6/1/11 |
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