Neurotoxicity of zearalenone’s metabolites and beauvericin mycotoxins via apoptosis and cell cycle disruption

Toxicology ◽  
2021 ◽  
pp. 152784
Author(s):  
Fojan Agahi ◽  
Cristina Juan ◽  
Guillermina Font ◽  
Ana Juan-García
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Disruption

scholarly journals Selective antisense oligonucleotide inhibition of human IRF4 prevents malignant myeloma regeneration via cell cycle disruption

2021 ◽  
Author(s):  
Phoebe K. Mondala ◽  
Ashni A. Vora ◽  
Tianyuan Zhou ◽  
Elisa Lazzari ◽  
Luisa Ladel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Antisense Oligonucleotide ◽  
Cell Cycle Disruption

scholarly journals The Human Transcriptome During Nontyphoid Salmonella and HIV Coinfection Reveals Attenuated NFκB-Mediated Inflammation and Persistent Cell Cycle Disruption

2011 ◽  
Vol 204 (8) ◽  
pp. 1237-1245 ◽  
Author(s):  
Fernanda Schreiber ◽  
David J. Lynn ◽  
Angela Houston ◽  
Joanna Peters ◽  
Gershom Mwafulirwa ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Human Transcriptome ◽  
Hiv Coinfection ◽  
Cell Cycle Disruption ◽  
Persistent Cell

Targeted Modulation of FAK/PI3K/PDK1/AKT and FAK/p53 Pathways by Cucurbitacin B for the Antiproliferation Effect Against Human Cholangiocarcinoma Cells

2020 ◽  
Vol 48 (06) ◽  
pp. 1475-1489
Author(s):  
Sirinapha Klungsaeng ◽  
Veerapol Kukongviriyapan ◽  
Auemduan Prawan ◽  
Sarinya Kongpetch ◽  
Laddawan Senggunprai
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Tyrosine Kinases ◽  
Molecular Mechanisms ◽  
Inhibitory Effect ◽  
Chemotherapeutic Agents ◽  
Cucurbitacin B ◽  
M Phase ◽  
Cell Cycle Disruption

Inadequate responses to traditional chemotherapeutic agents in cholangiocarcinoma (CCA) emphasize a requirement for new effective compounds for the treatment of this malignancy. This study aimed to investigate the antiproliferative property of cucurbitacin B on KKU-100 CCA cells. The determination of underlying molecular mechanisms was also carried out. The results revealed that cucurbitacin B suppressed growth and replicative ability to form colonies of CCA cells, suggesting the antiproliferative effect of this compound against the cells. Flow cytometry analysis demonstrated that the interfering effect of cucurbitacin B on the CCA cell cycle at the G2/M phase was accountable for its antiproliferation property. Accompanied with cell cycle disruption, cucurbitacin B altered the expression of proteins involved in the G2/M phase transition including downregulation of cyclin A, cyclin D1, and cdc25A, and upregulation of p21. Additional molecular studies demonstrated that cucurbitacin B suppressed the activation of focal adhesion kinase (FAK) which consequently resulted in inhibition of its kinase-dependent and kinase-independent downstream targets contributing to the regulation of cell proliferation including PI3K/PDK1/AKT and p53 proteins. In this study, the transient knockdown of FAK using siRNA was employed to ascertain the role of FAK in CCA cell proliferation. Finally, the effect of cucurbitacin B on upstream receptor tyrosine kinases regulating FAK activation was elucidated. The results showed that the inhibitory effect of cucurbitacin B on FAK activation in CCA cells is mediated via interference of EGFR and HER2 expression. Collectively, cucurbitacin B might be a promising drug for CCA treatment by targeting FAK protein.

Nuclear failure, DNA damage, and cell cycle disruption after migration through small pores: a brief review

2019 ◽  
Vol 63 (5) ◽  
pp. 569-577
Author(s):  
Charlotte R. Pfeifer ◽  
Manasvita Vashisth ◽  
Yuntao Xia ◽  
Dennis E. Discher
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Local Density ◽  
Nuclear Lamina ◽  
Nuclear Deformation ◽  
Nuclear Factors ◽  
A Cell ◽  
Dense Tissue ◽  
Cell Cycle Disruption ◽  
Dependent Processes

Abstract In many contexts of development, regeneration, or disease such as cancer, a cell squeezes through a dense tissue or a basement membrane, constricting its nucleus. Here, we describe how the severity of nuclear deformation depends on a nucleus’ mechanical properties that are mostly determined by the density of chromatin and by the nuclear lamina. We explain how constriction-induced nuclear deformation affects nuclear contents by causing (i) local density changes in chromatin and (ii) rupture of the nuclear lamina and envelope. Both processes mislocalize diffusible nuclear factors including key DNA repair and regulatory proteins. Importantly, these effects of constricted migration are accompanied by excess DNA damage, marked by phosphorylated histone γH2AX in fixed cells. Rupture has a number of downstream consequences that include a delayed cell cycle—consistent with a damage checkpoint—and modulation of differentiation, both of which are expected to affect migration-dependent processes ranging from wound healing to tumorigenic invasion.

scholarly journals Impact of Cell Cycle Disruption on Impaired Hepatic Regeneration in Aged Livers with Ischemic Insult

2012 ◽  
Vol 173 (2) ◽  
pp. 267-277 ◽  
Author(s):  
Atsushi Suzuki ◽  
Takanori Sakaguchi ◽  
Keisuke Inaba ◽  
Shohachi Suzuki ◽  
Hiroyuki Konno
Keyword(s):  
Cell Cycle ◽  
Hepatic Regeneration ◽  
Ischemic Insult ◽  
Cell Cycle Disruption

Selective Antisense Oligonucleotide Inhibition of Human IRF4 Prevents Malignant Myeloma Regeneration Via Cell Cycle Disruption

2020 ◽  
Author(s):  
Phoebe K. Mondala ◽  
Ashni A. Vora ◽  
Tianyuan Zhou ◽  
Elisa Lazzari ◽  
Luisa Ladel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Antisense Oligonucleotide ◽  
Cell Cycle Disruption

scholarly journals The Antibiotic Monensin Causes Cell Cycle Disruption ofToxoplasma gondiiMediated through the DNA Repair Enzyme TgMSH-1

2010 ◽  
Vol 55 (2) ◽  
pp. 745-755 ◽  
Author(s):  
Mark D. Lavine ◽  
Gustavo Arrizabalaga
Keyword(s):  
Cell Cycle ◽  
Mode Of Action ◽  
Drug Susceptibility ◽  
Cell Cycle Checkpoint ◽  
Phase Cell ◽  
Repair Enzyme ◽  
Coccidian Parasites ◽  
Cycle Checkpoint ◽  
Dependent Cell ◽  
Cell Cycle Disruption

ABSTRACTMonensin is a polyether ionophore antibiotic that is widely used in the control of coccidia in animals. Despite its significance in veterinary medicine, little is known about its mode of action and potential mechanisms of resistance in coccidian parasites. Here we show that monensin causes accumulation of the coccidianToxoplasma gondiiat an apparent late-S-phase cell cycle checkpoint. In addition, experiments utilizing a monensin-resistantT. gondiimutant show that this effect of monensin is dependent on the function of a mitochondrial homologue of the MutS DNA damage repair enzyme (TgMSH-1). Furthermore, the same TgMSH-1-dependent cell cycle disruption is observed with the antiparasitic ionophore salinomycin and the DNA alkylating agent methyl nitrosourea. Our results suggest a novel mechanism for the mode of action of monensin and salinomycin on coccidial parasites, in which the drug activates an MSH-1-dependent cell cycle checkpoint by an unknown mechanism, ultimately leading to the death of the parasite. This model would indicate that cell cycle disruption is an important mediator of drug susceptibility and resistance to ionophoric antibiotics in coccidian parasites.

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