Search results for "Cell cycle control"

showing 5 items of 5 documents

CHK1-targeted therapy to deplete DNA replication-stressed, p53-deficient, hyperdiploid colorectal cancer stem cells.

2017

ObjectiveCancer stem cells (CSCs) are responsible for tumour formation and spreading, and their targeting is required for tumour eradication. There are limited therapeutic options for advanced colorectal cancer (CRC), particularly for tumours carrying RAS-activating mutations. The aim of this study was to identify novel CSC-targeting strategies.DesignTo discover potential therapeutics to be clinically investigated as single agent, we performed a screening with a panel of FDA-approved or investigational drugs on primary CRC cells enriched for CSCs (CRC-SCs) isolated from 27 patients. Candidate predictive biomarkers of efficacy were identified by integrating genomic, reverse-phase protein mic…

0301 basic medicinep53DNA ReplicationCELL CYCLE CONTROLDNA damageColorectal cancerColonmedicine.medical_treatmentAntineoplastic AgentsBiologyBioinformaticsmedicine.disease_causeDNA DAMAGETargeted therapy03 medical and health sciencesCancer stem cellCell Line TumormedicineHumansCHEK11506DRUG DEVELOPMENTOligonucleotide Array Sequence AnalysisMutationCOLORECTAL CANCERSettore MED/06 - ONCOLOGIA MEDICAGastroenterologyCHEMOTHERAPYmedicine.diseaseImmunohistochemistryPrexasertib030104 developmental biologyPyrazinesCheckpoint Kinase 1MutationCancer researchNeoplastic Stem CellsPyrazolesStem cellTumor Suppressor Protein p53Colorectal NeoplasmsGut
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TCDD deregulates contact inhibition in rat liver oval cells via Ah receptor, JunD and cyclin A.

2007

The aryl hydrocarbon receptor (AhR) is a transcription factor involved in physiological processes, but also mediates most, if not all, toxic responses to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Activation of the AhR by TCDD leads to its dimerization with aryl hydrocarbon nuclear translocator (ARNT) and transcriptional activation of several phase I and II metabolizing enzymes. However, this classical signalling pathway so far failed to explain the pleiotropic hazardous effects of TCDD, such as developmental toxicity and tumour promotion. Thus, there is an urgent need to define genetic programmes orchestrated by AhR to unravel its role in physiology and toxicology. Here we show that TCDD …

Cancer ResearchAryl hydrocarbon receptor nuclear translocatorPolychlorinated Dibenzodioxinscyclin AProto-Oncogene Proteins c-junCyclin DCyclin Acell cycle controlCyclin ATetrachlorodibenzodioxinModels BiologicalDownregulation and upregulationGeneticsAnimalsRNA Small InterferingMolecular BiologyTranscription factorAryl hydrocarbon receptorCells CulturedbiologyContact InhibitionContact inhibitionCell cycleAryl hydrocarbon receptorRatsAdult Stem CellsLiverReceptors Aryl Hydrocarbonliver oval cellsbiology.proteinCancer researchJunDOncogene
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Cargo transport through the nuclear pore complex at a glance.

2021

ABSTRACT Bidirectional transport of macromolecules across the nuclear envelope is a hallmark of eukaryotic cells, in which the genetic material is compartmentalized inside the nucleus. The nuclear pore complex (NPC) is the major gateway to the nucleus and it regulates nucleocytoplasmic transport, which is key to processes including transcriptional regulation and cell cycle control. Accordingly, components of the nuclear transport machinery are often found to be dysregulated or hijacked in diseases. In this Cell Science at a Glance article and accompanying poster, we provide an overview of our current understanding of cargo transport through the NPC, from the basic transport signals and mach…

Cell Nucleus0303 health sciencesBidirectional transportNuclear EnvelopeActive Transport Cell NucleusCell BiologyBiologyCell biologyNuclear Pore Complex Proteins03 medical and health sciences0302 clinical medicinemedicine.anatomical_structureEukaryotic CellsNucleocytoplasmic TransportCell cycle controlmedicineTranscriptional regulationNuclear PoreNuclear transportMultivalent bindingNuclear poreNucleus030217 neurology & neurosurgery030304 developmental biologyJournal of cell science
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Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
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Cancer cell(s) cycle sequencing reveals universal mechanisms of apoptosis

2010

In this paper, cell cycle in higher eukaryotes and their molecular networks signals both in G 1/S and G2/M transitions are replicated in silico. Biochemical kinetics, converted into a set of differential equations, and system control theory are employed to design multi-nested digital layers to simulate protein-to-protein activation and inhibition for cell cycle dynamics in the presence of damaged genomes. Sequencing and controlling the digital process of four micro-scale species networks (p53/Mdm2/DNA damage, p21mRNA/cyclin-CDK complex, CDK/CDC25/wee1/ SKP2/APC/CKI and apoptosis target genes system) not only allows the comprehension of the mechanisms of these molecule interactions but paves…

Settore ING-IND/06 - Fluidodinamicacell digital biotechnology cancer cell cycle control cell digital systems protein networks signalling apoptosis
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