Search results for " Cell Cycle"

showing 10 items of 92 documents

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
researchProduct

Molecular mechanisms of sorafenib action in liver cancer cells.

2012

Sorafenib, a multikinase inhibitor, recently received FDA approval for the treatment of advanced hepatocellular carcinoma (HCC). However, as the clinical application of sorafenib evolves, there is increasing interest in defining the mechanisms underlying its anti-tumor activity. Considering that this specific inhibitor could target unexpected molecules depending on the biologic context, a precise understanding of its mechanism of action could be critical to maximize its treatment efficacy, while minimizing adverse effects. Two human HCC cell lines (HepG2 and Huh7), carrying different biological and genetic characteristics, were used in this study to examine the intracellular events leading …

SorafenibDNA ReplicationNiacinamideCarcinoma HepatocellularDNA RepairTranscription GeneticAngiogenesisCell SurvivalPyridinesApoptosisPharmacologyBiologysorafenib HCC mini-chromosome maintenance genes Dickkopf1 Harakiri Acheron/LARP6 YAP1 cell cycle microarray global gene expression analysisCell Line TumormedicineCell AdhesionHumansneoplasmsMolecular BiologyProtein Kinase InhibitorsCell ProliferationYAP1Neovascularization PathologicCell growthGene Expression ProfilingPhenylurea CompoundsBenzenesulfonatesCell CycleLiver NeoplasmsBiological TransportCell BiologyCell cycleSorafenibmedicine.diseasedigestive system diseasesMechanism of actionHepatocellular carcinomaProtein Biosynthesismedicine.symptomMitogen-Activated Protein KinasesLiver cancerDevelopmental Biologymedicine.drugSignal Transduction
researchProduct

Identification of a Terphenyl Derivative that Blocks the Cell Cycle in the G0−G1 Phase and Induces Differentiation in Leukemia Cells

2006

To further explore the SAR of resveratrol-related trans-stilbene derivatives, here we describe the synthesis of (a) a series of 3,5-dimethoxy analogues in which a variety of substituents were introduced at positions 2', 3', 4', and 5' of the stilbene scaffold and (b) a second group of derivatives (2-phenylnaphthalenes and terphenyls) that incorporate a phenyl ring as a bioisosteric replacement of the stilbene alkenyl bridge. We thoroughly characterized all of the new compounds with respect to their apoptosis-inducing activity and their effects on the cell cycle. One of the new derivatives, 13g, behaved differently from the others, as it was able to block the cell cycle in the G(0)-G(1) phas…

StereochemistryCellular differentiationFusion Proteins bcr-ablAntineoplastic AgentsApoptosis.ResveratrolResting Phase Cell CycleChemical synthesisStructure-Activity Relationshipchemistry.chemical_compoundLeukemia Promyelocytic AcuteCell Line TumorTerphenyl CompoundsTerphenylStilbenesDrug DiscoveryHumansStructure–activity relationshipATP Binding Cassette Transporter Subfamily B Member 1G1 PhaseCell DifferentiationCell cycleIn vitrochemistryDrug Resistance NeoplasmResveratrolCell cultureMolecular MedicineDrug Screening Assays AntitumorJournal of Medicinal Chemistry
researchProduct

Gold(I) Biscarbene Complexes Derived from Vascular-Disrupting Combretastatin A-4 Address Different Targets and Show Antimetastatic Potential

2014

Gold N-heterocyclic carbene (NHC) complexes are an emerging class of anticancer drugs. We present a series of gold(I) biscarbene complexes with NHC ligands derived from the plant metabolite combretastatin A-4 (CA-4) that retain its vascular-disrupting effect, yet address different cellular and protein targets. Unlike CA-4, these complexes did not interfere with tubulin, but with the actin cytoskeleton of endothelial and cancer cells. For the highly metastatic 518A2 melanoma cell line this effect was accompanied by a marked accumulation of cells in the G1 phase of the cell cycle and a suppression of active prometastatic matrix metalloproteinase-2. Despite these mechanistic differences the co…

StereochemistryNeovascularization PhysiologicAntineoplastic AgentsBiologyBiochemistryMicechemistry.chemical_compoundCoordination ComplexesTubulinCell Line TumorBibenzylsDrug DiscoveryHuman Umbilical Vein Endothelial CellsAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsMelanomaCell ProliferationPharmacologyCombretastatin A-4Tube formationCombretastatinMice Inbred BALB COrganic ChemistryCell cycleActin cytoskeletonG2 Phase Cell Cycle CheckpointsActin CytoskeletonChorioallantoic membranechemistryDrug Resistance NeoplasmCell cultureCancer cellMCF-7 CellsCancer researchMolecular MedicineGoldHT29 CellsMethaneChemMedChem
researchProduct

Let-7d miRNA Shows Both Antioncogenic and Oncogenic Functions in Osteosarcoma-Derived 3AB-OS Cancer Stem Cells

2015

Osteosarcoma (OS), an aggressive highly invasive and metastatic bone-malignancy, shows therapy resistance and recurrence, two features that likely depend on cancer stem cells (CSCs), which hold both self-renewing and malignant potential. So, effective anticancer therapies against OS should specifically target and destroy CSCs. We previously found that the let-7d microRNA was downregulated in the 3AB-OS-CSCs, derived from the human OS-MG63 cells. Here, we aimed to assess whether let-7d modulation affected tumorigenic and stemness properties of these OS-CSCs. We found that let-7d-overexpression reduced cell proliferation by decreasing CCND2 and E2F2 cell-cycle-activators and increasing p21 an…

Time FactorsEpithelial-Mesenchymal TransitionTime FactorTranscription FactorPhysiologyClinical BiochemistryDrug ResistanceAntineoplastic AgentsApoptosisBone NeoplasmsCell Cycle ProteinsBone NeoplasmTransfectionCell LineAntineoplastic AgentCell MovementCell Line TumorCell Cycle ProteinHumansNeoplasm InvasivenessCell Self RenewalAntineoplastic Agents; Apoptosis; Apoptosis Regulatory Proteins; Bone Neoplasms; Cell Cycle; Cell Cycle Proteins; Cell Line Tumor; Cell Movement; Cell Self Renewal; Drug Resistance Neoplasm; Epithelial-Mesenchymal Transition; Gene Expression Regulation Neoplastic; Humans; MicroRNAs; Neoplasm Invasiveness; Neoplastic Stem Cells; Osteosarcoma; Phenotype; Signal Transduction; Time Factors; Transcription Factors; Transfection; Physiology; Medicine (all); Clinical Biochemistry; Cell BiologyNeoplasm InvasiveneNeoplasticOsteosarcomaTumorApoptosis Regulatory ProteinMedicine (all)Cell CycleApoptosiMicroRNACell BiologyGene Expression Regulation NeoplasticMicroRNAsPhenotypeGene Expression RegulationDrug Resistance NeoplasmNeoplastic Stem CellsNeoplasmNeoplastic Stem CellApoptosis Regulatory ProteinsTranscription FactorsHumanSignal Transduction
researchProduct

Epigenetic activation of a cryptic TBC1D16 transcript enhances melanoma progression by targeting EGFR

2015

Metastasis is respoMetastasis is responsible for most cancer-related deaths, and, among common tumor types, melanoma is one with great potential to metastasize. Here we study the contribution of epigenetic changes to the dissemination process by analyzing the changes that occur at the DNA methylation level between primary cancer cells and metastases. We found a hypomethylation event that reactivates a cryptic transcript of the Rab GTPase activating protein TBC1D16 (TBC1D16-47 kDa; referred to hereafter as TBC1D16-47KD) to be a characteristic feature of the metastatic cascade. This short isoform of TBC1D16 exacerbates melanoma growth and metastasis both in vitro and in vivo. By combining imm…

Transcriptional ActivationGTPase-activating proteinImmunoprecipitationMice NudeEditorials: Cell Cycle FeaturesBiologyBioinformaticsMethylationGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticMetastasisMetastasisEpigènesiMetàstasiCell Line TumormedicineAnimalsImmunoprecipitationProtein IsoformsRNA MessengerEpigeneticsNeoplasm MetastasisRNA Small InterferingPromoter Regions GeneticProteïnes supressores de tumorsProtein Kinase InhibitorsMelanomaMelanomaGTPase-Activating ProteinsGeneral MedicineMethylationDNA MethylationPrognosismedicine.diseaseTumor suppressor proteinErbB ReceptorsMolecular WeightTreatment Outcomerab GTP-Binding ProteinsDNA methylationDisease ProgressionCancer researchRabMetilacióProtein BindingSignal TransductionEpigenesisNature Medicine
researchProduct

Exploring the anticancer potential of pyrazolo[1,2-a]benzo[1,2,3,4] tetrazin-3-one derivatives: The effect on apoptosis induction, cell cycle and pro…

2013

In order to investigate their anticancer potential, four new pyrazolo[1,2-a]benzo[1,2,3,4]-tetrazinone derivatives, designed through the chemometric protocol VLAK, and three of the most active compounds of the previous series have been evaluated on some cellular events including proliferation, apoptosis induction, and cell cycle. The NCI one dose (10 mu M) screening revealed that the 8,9-di-methyl derivative showed activity against Leukemia (CCRF-CEM) and Colon cancer cell line (COLO 205), reaching 81% and 45% of growth inhibition (GI), respectively. Replacement of the two methyl groups with two chlorine atoms maintained the activity toward Leukemia cell (CCRF-CEM, GI 77%) and selectively e…

VLAK protocolStereochemistryCell Survival3Cell2Pyrazolo[1Antineoplastic AgentsApoptosisCell cycleHeLachemistry.chemical_compoundStructure-Activity RelationshipPyrazolo[12-a]benzo[1234]tetrazinone VLAK protocol Anticancer agents Apoptosis inducers Cell cycleCell Line TumorDrug DiscoverymedicineHumans2-a]benzo[1EC50Cell ProliferationPharmacologybiologyDose-Response Relationship DrugMolecular StructureCell growthOrganic ChemistryApoptosis inducers4]tetrazinoneGeneral MedicineCell cyclebiology.organism_classificationmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaLeukemiamedicine.anatomical_structurechemistryApoptosisAnticancer agentsCancer researchGrowth inhibitionHeterocyclic Compounds 3-RingHeLa Cells
researchProduct

Synthesis of Combretastatin A-4 and 3′-Aminocombretastatin A-4 derivatives with Aminoacid Containing Pendants and Study of their Interaction with Tub…

2020

Natural product combretastatin A-4 (CA-4) and its nitrogenated analogue 3&prime

Vascular Endothelial Growth Factor ACell cycle checkpoint<i>htert</i>Pharmaceutical ScienceApoptosisAnalytical Chemistrychemistry.chemical_compound0302 clinical medicineDrug DiscoveryStilbenesc-<i>myc</i>Telomerase0303 health sciences<i>vegf</i>biologyNeovascularization PathologicChemistry3′-aminocombretastatin a-4Cell cycle<i>c-Myc</i>VEGFc-MycBiochemistryChemistry (miscellaneous)030220 oncology & carcinogenesisMCF-7 CellsMolecular Medicinecytotoxicitycell cyclehTERTHT29 CellsArticleProto-Oncogene Proteins c-mycmicrotubuleslcsh:QD241-44103 medical and health sciencesStructure-Activity Relationshiplcsh:Organic chemistryMicrotubuleCell Line TumorHumansPhysical and Theoretical Chemistry030304 developmental biologyCell ProliferationCombretastatinCombretastatin A-4Cell growthOrganic ChemistryAntineoplastic Agents PhytogenicTubulintubulinCell cultureA549 Cellsbiology.proteinM Phase Cell Cycle Checkpointscombretastatin a-4Drug Screening Assays AntitumorMolecules
researchProduct

Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
researchProduct

Depletion ofL-arginine induces autophagy as a cytoprotective response to endoplasmic reticulum stress in human T lymphocytes

2012

PMCID: PMC3494587

X-Box Binding Protein 1Proteasome Endopeptidase ComplexProgrammed cell deathXBP1CD3 ComplexMAP Kinase Signaling SystemRNA SplicingT-LymphocytesT cellDown-RegulationApoptosisRegulatory Factor X Transcription FactorsUbiquitin-Activating EnzymesProtein Serine-Threonine KinasesBiologyArginineLymphocyte ActivationAutophagy-Related Protein 7Jurkat cellsJurkat CellsEndoribonucleasesAutophagymedicineHumansMolecular BiologyCell ProliferationTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCell BiologyBECN1Endoplasmic Reticulum StressG1 Phase Cell Cycle CheckpointsBasic Research Paper3. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureCytoprotectionApoptosisUnfolded protein responseBeclin-1MitogensApoptosis Regulatory ProteinsLysosomesProto-Oncogene Proteins c-aktTranscription FactorsAutophagy
researchProduct