Mitotic Catastrophe Results in Cell Death by Caspase-Dependentand Caspase-Independent Mechanisms

@article{Mansilla2006MitoticCR,
  title={Mitotic Catastrophe Results in Cell Death by Caspase-Dependentand Caspase-Independent Mechanisms},
  author={Sylvia Mansilla and W. Priebe and J. Portugal},
  journal={Cell Cycle},
  year={2006},
  volume={5},
  pages={53 - 60}
}
Exposure of MDA-MB-231 and MCF-7/VP human breast carcinoma cells to theanthracyclines doxorubicin and WP631 induced polyploidy, formation of multinucleated cellsand cell death by mitotic catastrophe through caspase-dependent and caspase-independentmechanisms. In both cell lines, the antiproliferative effect of WP631 was higher than that ofdoxorubicin and a transient halt in G2/M was observed without cell senescence, while p53-dependent apoptosis did not occur in these cells. Mitotic catastrophe… Expand
Apoptotic-like death occurs through a caspase-independent route in colon carcinoma cells undergoing mitotic catastrophe.
TLDR
Lack of p53 facilitated endoreduplication and polyploidy in PTX-treated cells, but cells were still killed with similar efficacy through the same apoptotic-like mechanism in the absence of caspase activity. Expand
DNA damage induces two distinct modes of cell death in ovarian carcinomas
TLDR
It is hypothesized that the final mode of cell death triggered by DNA damage in ovarian carcinoma cells is determined by the profile of proteins involved in the regulation of the cell cycle, such as p53- and Chk2-related proteins. Expand
The adenovirus E4orf4 protein induces growth arrest and mitotic catastrophe in H1299 human lung carcinoma cells
TLDR
In the present studies using H1299 human lung carcinoma cells as a model system, death is induced in the absence of activation of any of the caspases tested, accumulation of reactive oxygen species, or release of cytochrome c from mitochondria. Expand
Mithramycin SK modulates polyploidy and cell death in colon carcinoma cells
TLDR
Treatment of HCT-116 (p53+/+) colon carcinoma cells with the novel antitumor antibiotic mithramycin SK (MSK) results in polyploidization and mitotic catastrophe, which occurs after a transient halt in G1 phase followed by the overtaking of the G2-M checkpoint when treated cells are incubated in a fresh drug-free medium. Expand
Cellular response and activation of apoptosis by mithramycin SK in p21(WAF1)-deficient HCT116 human colon carcinoma cells.
TLDR
HCT116 (p21(-/-)) human colon carcinoma cells treated with mithramycin SK (MSK) were transiently arrested in G2/M, with some cells entering a faulty mitotic cycle without cytokinesis that resulted in G1-like cell arrest, which consisted of post-mitotic aneuploid G1 cells. Expand
Caspase-2 is involved in cell death induction by taxanes in breast cancer cells
TLDR
Caspase-2 is required, at least partially, for apoptosis induction by taxanes in tested breast cancer cells, and it is suggested that caspasing-2 plays the role of an apical caspase in these cells. Expand
Involvement of Centrosome Amplification in Radiation-Induced Mitotic Catastrophe
TLDR
A significant proportion of cell death induced by ionising irradiation is through an apoptosis-independent mechanism involving centrosome amplification and mitotic catastrophe, demonstrating that a major proportion of cells exposed to ionising radiation die via different mechanisms. Expand
Sequential induction of mitotic catastrophe followed by apoptosis in human leukemia MOLT4 cells by imidazoacridinone C-1311
TLDR
Findings show that C-1311-induced mitotic catastrophe is not the ultimate death event but rather a step precipitating delayed, albeit massive, apoptotic responses. Expand
Transcriptional changes facilitate mitotic catastrophe in tumour cells that contain functional p53.
TLDR
The results suggest that WP631 induced changes in cell cycle control pathways leading to death of Jurkat T cells through mitotic catastrophe, which occurred in the absence of caspase-2 and caspases-3 activities, rather than apoptosis. Expand
Mitotic catastrophe induced in HeLa cells by photodynamic treatment with Zn(II)-phthalocyanine.
TLDR
The results in p53-deficient human cervix carcinoma HeLa cells subjected to sublethal PDT treatments using Zn(II)-phthalocyanine incorporated into liposomes are presented, to the authors' knowledge, the first description of this cell death modality after PDT with ZnPc. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 56 REFERENCES
Influence of p53 and caspase 3 activity on cell death and senescence in response to methotrexate in the breast tumor cell.
TLDR
It is suggested that the nature of the cellular response to methotrexate depends, in large part, on p53 and caspase function, and that the senescence phenotype may occur in the absence of direct DNA damage. Expand
Apoptosis Resistance of MCF-7 Breast Carcinoma Cells to Ionizing Radiation Is Independent of p53 and Cell Cycle Control but Caused by the Lack of Caspase-3 and a Caffeine-Inhibitable Event
We have shown previously that ionizing radiation (IR) induces a persistent G2-M arrest but not cell death in MCF-7 breast carcinoma cells that harbor functional p53 but lack caspase-3. In the presentExpand
Two distinct modes of cell death induced by doxorubicin: apoptosis and cell death through mitotic catastrophe accompanied by senescence-like phenotype
TLDR
Results indicate that different doses of doxorubicin activate different regulatory mechanisms to induce either apoptosis or cell death through mitotic catastrophe. Expand
Mitotic catastrophe constitutes a special case of apoptosis whose suppression entails aneuploidy
TLDR
A molecular pathway through which DNA damage, failure to arrest the cell cycle and inhibition of apoptosis can favor the occurrence of cytogenetic abnormalities that are likely to participate in oncogenesis is delineated. Expand
Early caspase activation in leukemic cells subject to etoposide-induced G2-M arrest: evidence of commitment to apoptosis rather than mitotic cell death.
  • R. J. Sleiman, B. Stewart
  • Biology, Medicine
  • Clinical cancer research : an official journal of the American Association for Cancer Research
  • 2000
TLDR
The present data suggest that commitment to apoptosis occurs in parallel to G2-M arrest in leukemic cells, and the impact of caffeine on cytotoxicity under these conditions. Expand
Dual modes of death induced by etoposide in human epithelial tumor cells allow Bcl-2 to inhibit apoptosis without affecting clonogenic survival.
TLDR
Although Bcl-2 inhibited etoposide-induced apoptosis, it had no effect on the formation of giant, multinucleated cells characteristic of mitotic catastrophe, indicating that the ability of B cl-2 to prevent apoptosis caused by chemotherapeutic drugs may not necessarily translate into increased survival of cells that express Bcl.2. Expand
Caspase inhibition switches doxorubicin-induced apoptosis to senescence
TLDR
The findings suggest that the inhibition of apoptosis may lead to an increased expression of cell cycle inhibitors and cellular senescence. Expand
Involvement of p21 in mitotic exit after paclitaxel treatment in MCF-7 breast adenocarcinoma cell line
TLDR
It is shown that paclitaxel induced accumulation of p21 in cells with a G2/M DNA content, corresponding to cells either in abnormal mitosis or in an interphase-like state (decondensed chromatin) with multiple nuclei, which effectively enhances cell survival after pac litaxel-induced spindle damage. Expand
Apoptosis and cell recovery in response to oxidative stress in p53-deficient prostate carcinoma cells.
TLDR
Whether apoptotic response to the oxidative insult was altered such that, unlike in cells containing functional p53 apoptosis, it may be reduced and replaced by other mechanisms of cellular arrest and death is sought. Expand
If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells.
  • I. Roninson, E. Broude, B. Chang
  • Biology, Medicine
  • Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
  • 2001
TLDR
The senescent phenotype distinguishes tumor cells that survived drug exposure but lost the ability to form colonies from those that recover and proliferate after treatment, and should assist in improving the efficacy and decreasing side effects of cancer therapy. Expand
...
1
2
3
4
5
...