If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells

Roninson, Igor B.; Broude, Eugenia V.; Chang, Bey-Dih

doi:10.1054/drup.2001.0213

Cited by 658 publications

(610 citation statements)

References 80 publications

Supporting

Mentioning

569

Contrasting

Unclassified

Order By: Relevance

“…8 Moreover, the relationship between radiation-induced G2/M delay and the cellular response to ionizing radiation has been studied extensively. 27,33,34 While examining the mechanisms of this survival effect of RhoB-F, we have further demonstrated that radioresistant RhoB-F cells exhibited a more marked G2/M arrest than RhoB-GG cells, strongly implicating RhoB-F in the control of mechanisms of mitotic entry or the mitotic checkpoint following irradiation.…”

Section: Discussionmentioning

confidence: 99%

“…26,27 Furthermore, it has been largely reported that this G2 checkpoint is particularly important in preventing mitotic catastrophe in cells exposed to DNA damage (for a review, See Roninson et al 8 ). We therefore compared the effect of expressing either RhoB-F or RhoB-GG on radiation-induced G2/M arrest.…”

Section: Rhob-f Cells Displayed An Increased G2 Arrest Following Irramentioning

confidence: 99%

“…Such mitoses that fail to produce correct chromosomal segregation lead to the formation of large nonviable cells with several nuclei. 8 The appearance of these giant multinucleated cells, and, in consequence, mitotic cell death, has recently been associated with an abnormality of centrosomal duplication during the cell cycle following irradiation. 9,10 However, despite these recent data, the molecular mechanisms controlling this type of cell death are still largely unknown.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Farnesylated RhoB inhibits radiation-induced mitotic cell death and controls radiation-induced centrosome overduplication

et al. 2005

View full text Add to dashboard Cite

Our previous results demonstrated that expressing the GTPase ras homolog gene family, member B (RhoB) in radiosensitive NIH3T3 cells increases their survival following 2 Gy irradiation (SF2). We have first demonstrated here that RhoB expression inhibits radiation-induced mitotic cell death. RhoB is present in both a farnesylated and a geranylgeranylated form in vivo. By expressing RhoB mutants encoding for farnesylated (RhoB-F cells), geranylgeranylated or the CAAX deleted form of RhoB, we have then shown that only RhoB-F expression was able to increase the SF2 value by reducing the sensitivity of these cells to radiation-induced mitotic cell death. Moreover, RhoB-F cells showed an increased G2 arrest and an inhibition of centrosome overduplication following irradiation mediated by the Rhokinase, strongly suggesting that RhoB-F may control centrosome overduplication during the G2 arrest after irradiation. Overall, our results for the first time clearly implicate farnesylated RhoB as a crucial protein in mediating cellular resistance to radiation-induced nonapoptotic cell death.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Rhob-f Cells Displayed An Increased G2 Arrest Following Irramentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Farnesylated RhoB inhibits radiation-induced mitotic cell death and controls radiation-induced centrosome overduplication

et al. 2005

View full text Add to dashboard Cite

show abstract

“…However, there is no broad consensus on the use of this term, [16][17][18] and the NCDD recommends instead the use of terms such as 'cell death preceded by multinucleation' or 'cell death occurring during the metaphase', which are more precise and more informative. It is clear, however, that cell death during metaphase may have nothing to do with a cytokinesis or chromosome segregation defect but may occur because of exposure of cells to apoptotic stimuli during mitosis.…”

Section: Mitotic Catastrophementioning

confidence: 99%

Classification of cell death: recommendations of the Nomenclature Committee on Cell Death

et al. 2005

View full text Add to dashboard Cite

“…Roninson et al . [65] defined mitotic catastrophe as a type of cell death resulting from abnormal mitosis, usually ending in the formation of nuclear envelopes around individual clusters of missegregated chromosomes. The result is the formation of large cells with multiple micronuclei and decondensed chromatin.…”

Section: The Podocyte’s Catastrophe: Lost Cell Cycle Controlmentioning

confidence: 99%

Podocyte Mitosis – A Catastrophe

Lasagni

Lazzeri²,

Shankland

et al. 2012

CMM

View full text Add to dashboard Cite

Podocyte loss plays a key role in the progression of glomerular disorders towards glomerulosclerosis and chronic kidney disease. Podocytes form unique cytoplasmic extensions, foot processes, which attach to the outer surface of the glomerular basement membrane and interdigitate with neighboring podocytes to form the slit diaphragm. Maintaining these sophisticated structural elements requires an intricate actin cytoskeleton. Genetic, mechanic, and immunologic or toxic forms of podocyte injury can cause podocyte loss, which causes glomerular filtration barrier dysfunction, leading to proteinuria. Cell migration and cell division are two processes that require a rearrangement of the actin cytoskeleton; this rearrangement would disrupt the podocyte foot processes, therefore, podocytes have a limited capacity to divide or migrate. Indeed, all cells need to rearrange their actin cytoskeleton to assemble a correct mitotic spindle and to complete mitosis. Podocytes, even when being forced to bypass cell cycle checkpoints to initiate DNA synthesis and chromosome segregation, cannot complete cytokinesis efficiently and thus usually generate aneuploid podocytes. Such aneuploid podocytes rapidly detach and die, a process referred to as mitotic catastrophe. Thus, detached or dead podocytes cannot be adequately replaced by the proliferation of adjacent podocytes. However, even glomerular disorders with severe podocyte injury can undergo regression and remission, suggesting alternative mechanisms to compensate for podocyte loss, such as podocyte hypertrophy or podocyte regeneration from resident renal progenitor cells. Together, mitosis of the terminally differentiated podocyte rather accelerates podocyte loss and therefore glomerulosclerosis. Finding ways to enhance podocyte regeneration from other sources remains a challenge goal to improve the treatment of chronic kidney disease in the future.

show abstract

If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells

Cited by 658 publications

References 80 publications

Farnesylated RhoB inhibits radiation-induced mitotic cell death and controls radiation-induced centrosome overduplication

Farnesylated RhoB inhibits radiation-induced mitotic cell death and controls radiation-induced centrosome overduplication

Classification of cell death: recommendations of the Nomenclature Committee on Cell Death

Podocyte Mitosis – A Catastrophe

Contact Info

Product

Resources

About