Endopolyploidy in irradiated p53‐deficient tumour cell lines: Persistence of cell division activity in giant cells expressing Aurora‐B kinase

@article{Erenpreisa2008EndopolyploidyII,
  title={Endopolyploidy in irradiated p53‐deficient tumour cell lines: Persistence of cell division activity in giant cells expressing Aurora‐B kinase},
  author={J. Erenpreisa and A. Ivanov and S. Wheatley and E. Kosmacek and F. Ianzini and A. P. Anisimov and M. Mackey and P. Davis and G. Plakhins and T. Illidge},
  journal={Cell Biology International},
  year={2008},
  volume={32}
}
Recent findings including computerised live imaging suggest that polyploidy cells transiently emerging after severe genotoxic stress (and named ‘endopolyploid cells’) may have a role in tumour regrowth after anti‐cancer treatment. Until now, mostly the factors enabling metaphase were studied in them. Here we investigate the mitotic activities and the role of Aurora‐B, in view of potential depolyploidisation of these cells, because Aurora‐B kinase is responsible for coordination and completion… Expand
The role of meiotic cohesin REC8 in chromosome segregation in gamma irradiation-induced endopolyploid tumour cells.
TLDR
Observations indicate that radiation-induced ETCs express features of meiotic cell divisions and that these may facilitate chromosome segregation and genome reduction. Expand
Up-regulation of the embryonic self-renewal network through reversible polyploidy in irradiated p53-mutant tumour cells.
TLDR
Observations indicate that irradiation-induced ETC up-regulate key components of germ-line cells, which potentially facilitate survival and propagation of the tumour cell population. Expand
Polyploid tumour cells elicit paradiploid progeny through depolyploidizing divisions and regulated autophagic degradation
TLDR
‘neotic’ ETC resulting from genotoxically damaged p53 function‐deficient tumour cells develop through a heteronuclear system differentiating the polyploid genome into rejuvenated ‘viable’ subcells and subnuclei, which become degraded and eliminated by autophagy. Expand
Activation of meiosis-specific genes is associated with depolyploidization of human tumor cells following radiation-induced mitotic catastrophe.
TLDR
It is reported here that cells undergoing radiation-induced MC are more plastic with regards to ploidy and that this plasticity allows them to reorganize their genetic material through reduction division to produce smaller cells which are morphologically indistinguishable from control cells. Expand
A nuclear budding mechanism in transiently arrested cells generates drug-sensitive and drug-resistant cells.
TLDR
Nuclear budding was accompanied by changes in protein levels in the giant cells, including inhibition of p53 and enhanced expression of p21(WAF1 and the meiosis-related Mos. Expand
Polyploidy formation in cancer cells: how a Trojan horse is born.
TLDR
It is proposed that modern anti-cancer therapies should be designed taking under consideration polyploidization/ depolyploidized processes, which confer the polyploidsization a hidden potential similar to a Trojan horse delayed aggressiveness. Expand
The Cancer Aneuploidy Paradox: In the Light of Evolution
TLDR
This cancer life-cycle has parallels both within the cycling polyploidy of the asexual life cycles of ancient unicellular protists and cleavage embryos of early multicellulars, supporting the atavistic theory of cancer. Expand
Volume increase and spatial shifts of chromosome territories in nuclei of radiation-induced polyploidizing tumour cells.
TLDR
The data suggest a radiation-induced generation of large intra-nuclear chromosome territories and their repositioning prior to genome reduction after irradiation in p53-function deficient HeLa cells. Expand
Self-Renewal Signalling in Presenescent Tetraploid IMR90 Cells
TLDR
A positive link between DDR, self-renewal, and senescence signalling is initiated in the cells overcoming the tetraploidy barrier, indicating that cellular and molecular context of induced tetraPloidy during this period of presenescence is favourable for carcinogenesis. Expand
Three steps to the immortality of cancer cells: senescence, polyploidy and self-renewal
TLDR
It is proposed that genotoxic resistance is thereby afforded through a programmed life-cycle-like process which intimately unites senescence, polyploidy and stemness. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 46 REFERENCES
POLYPLOID GIANT CELLS PROVIDE A SURVIVAL MECHANISM FOR p53 MUTANT CELLS AFTER DNA DAMAGE
TLDR
It is proposed that the formation of giant cells and their subsequent complex breakdown and subnuclear reorganization may represent an important response of p53‐mutated tumours to DNA damaging agents and provide tumours with a mechanism of repair and resistance to such treatments. Expand
Segregation of genomes in polyploid tumour cells following mitotic catastrophe
TLDR
The data presented indicate that endopolyploid tumour cells preserve the integrity of individual genomes and can potentially re‐initiate mitosis from the point at which it was interrupted. Expand
RELEASE OF MITOTIC DESCENDANTS BY GIANT CELLS FROM IRRADIATED BURKITT'S LYMPHOMA CELL LINES
TLDR
This process of giant cell formation, reorganization and breakdown appears to provide an additional mechanism for repairing double‐strand DNA breaks within tumour cells. Expand
Tetraploidy/aneuploidy and stem cells in cancer promotion: The role of chromosome passenger proteins
TLDR
It is intriguing to speculate that in some cancers, tetraploidy/aneuploidsy induced by deregulated expression of a mitotic regulator represents a primary event that leads to unbalanced expression ofA cluster of crucial genes and to cellular transformation. Expand
Endopolyploid cells produced after severe genotoxic damage have the potential to repair DNA double strand breaks
TLDR
It is suggested that after severe genotoxic insult endopolyploid cells have a transient survival advantage that may contribute to radioresistance of tumours that undergo mitotic catastrophe and endoreduplication is involved in selecting cells resistant to apoptosis. Expand
Mitotic Instability in Cancer: Is There Method in the Madness?
TLDR
The telomere-dependent instability can be partly counteracted by expression of telomerase during tumour progression, but genomic stabilisation is rarely, if ever, complete. Expand
Vascular smooth muscle cell polyploidization involves changes in chromosome passenger proteins and an endomitotic cell cycle.
TLDR
It is shown via time-lapse video imaging and immunofluorescence analyses that primary vascular smooth muscle cells (VSMC) undergo an endomitotic-type cell cycle, including a normal progression through part of mitosis, and that ectopically expressed Survivin inhibits polyploidization in vascular smoother muscle cells. Expand
Genesis and evolution of high‐ploidy tumour cells evaluated by means of the proliferation markers p34cdc2, cyclin B1, PCNA and 3[H]‐thymidine
TLDR
The results suggest that polyploid cells are not quiescent, their cell cycle is longer than that of the modal‐ploidy population, and they maintain cyclin B1 throughout the cycle, which may contribute to their genesis by impeding the exit from mitosis. Expand
Mitotic death: a mechanism of survival? A review
TLDR
The features of mitotic death do not simply represent aberrations of dying cells but are indicative of a switch to amitotic modes of cell survival that may provide additional mechanisms of genotoxic resistance. Expand
Polyploidization and exit from cell cycle as mechanisms of cultured melanoma cell resistance to methotrexate.
TLDR
The results indicate that methotrexate at a high dosage selects a cell population heterogeneous concerning its ploidy level, composed of one subpopulation of high-ploidy cells and another of modal-ploidsy cells that, considering its lack of CDK1 expression, would remain in a latent state to evade the effects of the drug. Expand
...
1
2
3
4
5
...