scholarly journals Chromothripsis: A Cause of Genome Instability in Cancer

2021 ◽  
Vol 3 (4) ◽  
pp. 5-11
Author(s):  
Ishita Agrawal ◽  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Growth ◽  
Genome Instability ◽  
Cell Cycle Checkpoint ◽  
Genetic Changes ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint

Cancer is a term given to uncontrolled cell growth, which is the result of accumulation of genetic changes during cell division. It can occur due to both genetic and environmental reasons. One such genetic cause of cancer discovered recently is known as Chromothripsis. It is defined as the fragmentation and rearrangement of chromosomes. Researchers are still trying to find the true mechanism underlying Chromothripsis. Two models have been significantly described; first one is the ‘micronuclei hypothesis’, which occurs as a result of chromosome mis-segregation during Mitosis. Second model is based on the ‘telomere crisis’, which occurs due to faulty telomerase enzyme and cell cycle checkpoint pathway. In this letter, we have tried to give brief information about the mechanisms behind Chromothripsis and their role in causing genome instability leading to cancer.

scholarly journals Centrosome Dynamics and Its Role in Inflammatory Response and Metastatic Process

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 629
Author(s):  
Massimo Pancione ◽  
Luigi Cerulo ◽  
Andrea Remo ◽  
Guido Giordano ◽  
Álvaro Gutierrez-Uzquiza ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rho Gtpases ◽  
Human Cancer ◽  
Genetic Disorders ◽  
Cell Cycle Checkpoint ◽  
Animal Cells ◽  
Normal Tissues ◽  
Checkpoint Pathway ◽  
New Findings ◽  
Cycle Checkpoint

Metastasis is a process by which cancer cells escape from the location of the primary tumor invading normal tissues at distant organs. Chromosomal instability (CIN) is a hallmark of human cancer, associated with metastasis and therapeutic resistance. The centrosome plays a major role in organizing the microtubule cytoskeleton in animal cells regulating cellular architecture and cell division. Loss of centrosome integrity activates the p38-p53-p21 pathway, which results in cell-cycle arrest or senescence and acts as a cell-cycle checkpoint pathway. Structural and numerical centrosome abnormalities can lead to aneuploidy and CIN. New findings derived from studies on cancer and rare genetic disorders suggest that centrosome dysfunction alters the cellular microenvironment through Rho GTPases, p38, and JNK (c-Jun N-terminal Kinase)-dependent signaling in a way that is favorable for pro-invasive secretory phenotypes and aneuploidy tolerance. We here review recent data on how centrosomes act as complex molecular platforms for Rho GTPases and p38 MAPK (Mitogen activated kinase) signaling at the crossroads of CIN, cytoskeleton remodeling, and immune evasion via both cell-autonomous and non-autonomous mechanisms.

scholarly journals An Intrinsic Cell Cycle Checkpoint Pathway Mediated by MEK and ERK in Drosophila

2006 ◽  
Vol 11 (4) ◽  
pp. 575-582 ◽  
Author(s):  
Vladic Mogila ◽  
Fan Xia ◽  
Willis X. Li
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint

scholarly journals The Maize Homologue of the Cell Cycle Checkpoint Protein MAD2 Reveals Kinetochore Substructure and Contrasting Mitotic and Meiotic Localization Patterns

1999 ◽  
Vol 145 (3) ◽  
pp. 425-435 ◽  
Author(s):  
Hong-Guo Yu ◽  
Michael G. Muszynski ◽  
R. Kelly Dawe
Keyword(s):  
Cell Cycle ◽  
Spindle Assembly ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Protein ◽  
Microtubule Attachment ◽  
Checkpoint Pathway ◽  
Outer Domain ◽  
Cycle Checkpoint ◽  
Mitosis And Meiosis ◽  
Meiosis I

We have identified a maize homologue of yeast MAD2, an essential component in the spindle checkpoint pathway that ensures metaphase is complete before anaphase begins. Combined immunolocalization of MAD2 and a recently cloned maize CENPC homologue indicates that MAD2 localizes to an outer domain of the prometaphase kinetochore. MAD2 staining was primarily observed on mitotic kinetochores that lacked attached microtubules; i.e., at prometaphase or when the microtubules were depolymerized with oryzalin. In contrast, the loss of MAD2 staining in meiosis was not correlated with initial microtubule attachment but was correlated with a measure of tension: the distance between homologous or sister kinetochores (in meiosis I and II, respectively). Further, the tension-sensitive 3F3/2 phosphoepitope colocalized, and was lost concomitantly, with MAD2 staining at the meiotic kinetochore. The mechanism of spindle assembly (discussed here with respect to maize mitosis and meiosis) is likely to affect the relative contributions of attachment and tension. We support the idea that MAD2 is attachment-sensitive and that tension stabilizes microtubule attachments.

scholarly journals Cell cycle-dependent recruitment of FtsN to the divisome in Escherichia coli

2021 ◽  
Author(s):  
Jaana Mannik ◽  
Sebastien Pichoff ◽  
Joseph Lutkenhaus ◽  
Jaan Mannik
Keyword(s):  
Escherichia Coli ◽  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Checkpoint ◽  
Second Stage ◽  
Cycle Checkpoint ◽  
Z Ring ◽  
Lag Period ◽  
Cycle Dependent ◽  
Rate Limiting

Cell division in Escherichia coli starts with the formation of an FtsZ protofilament network in the middle of the cell, the Z ring. However, only after a considerable lag period do the cells start to form a midcell constriction. The basis of this cell cycle checkpoint is yet unclear. The onset of constriction is dependent upon the arrival of so-called late divisome proteins, among which, FtsN is the last arriving essential one. The timing and dependency of FtsN arrival to the divisome, along with genetic evidence, suggests it triggers cell division. In this study, we used high throughput fluorescence microscopy to quantitatively determine the arrival of FtsN and the early divisome protein ZapA to midcell at a single-cell level during the cell cycle. Our data show that recruitment of FtsN coincides with the initiation of constriction within experimental uncertainties and that the relative fraction of ZapA/FtsZ reaches its highest value at this event. We also find that FtsN is recruited to midcell in two distinct temporal stages with septal peptidoglycan synthesis starting in the first stage and accelerating in the second stage, during which the amount of ZapA/FtsZ in the midcell decreases. In the presence of FtsA*, recruitment of FtsN becomes concurrent with the formation of the Z-ring, but constriction is still delayed indicating FtsN recruitment is not rate limiting, at least under these conditions. Finally, our data support the recently proposed idea that ZapA/FtsZ and FtsN are part of physically separate complexes in midcell throughout the whole septation process.

scholarly journals Diacerein retards cell growth of chondrosarcoma cells at the G2/M cell cycle checkpoint via cyclin B1/CDK1 and CDK2 downregulation

BMC Cancer ◽  
2015 ◽  
Vol 15 (1) ◽  
Author(s):  
Birgit Lohberger ◽  
Andreas Leithner ◽  
Nicole Stuendl ◽  
Heike Kaltenegger ◽  
Werner Kullich ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Cyclin B1 ◽  
Cell Cycle Checkpoint ◽  
M Cell ◽  
Cycle Checkpoint

scholarly journals Interactions between p53 and MDM2 in a mammalian cell cycle checkpoint pathway.

1994 ◽  
Vol 91 (7) ◽  
pp. 2684-2688 ◽  
Author(s):  
C. Y. Chen ◽  
J. D. Oliner ◽  
Q. Zhan ◽  
A. J. Fornace ◽  
B. Vogelstein ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mammalian Cell ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Mammalian Cell Cycle ◽  
Cycle Checkpoint

scholarly journals Saccharomyces cerevisiae as a Model System To Define the Chromosomal Instability Phenotype

2005 ◽  
Vol 25 (16) ◽  
pp. 7226-7238 ◽  
Author(s):  
Christopher D. Putnam ◽  
Vincent Pennaneach ◽  
Richard D. Kolodner
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Genome Instability ◽  
Human Cancer ◽  
Terminal Segment ◽  
Cell Cycle Checkpoint ◽  
Nonhomologous End Joining ◽  
End Joining ◽  
Cycle Checkpoint ◽  
Chromosome Fusions

ABSTRACT Translocations, deletions, and chromosome fusions are frequent events seen in cancers with genome instability. Here we analyzed 358 genome rearrangements generated in Saccharomyces cerevisiae selected by the loss of the nonessential terminal segment of chromosome V. The rearrangements appeared to be generated by both nonhomologous end joining and homologous recombination and targeted all chromosomes. Fifteen percent of the rearrangements occurred independently more than once. High levels of specific classes of rearrangements were isolated from strains with specific mutations: translocations to Ty elements were increased in telomerase-defective mutants, potential dicentric translocations and dicentric isochromosomes were associated with cell cycle checkpoint defects, chromosome fusions were frequent in strains with both telomerase and cell cycle checkpoint defects, and translocations to homolog genes were seen in strains with defects allowing homoeologous recombination. An analysis of human cancer-associated rearrangements revealed parallels to the effects that strain genotypes have on classes of rearrangement in S. cerevisiae.

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