Search results for "G1 Phase"

showing 10 items of 36 documents

Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition

2016

AbstractA fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved …

0301 basic medicineAcute promyelocytic leukemiaScienceEGFRRetinoic acidMice NudeTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundDifferentiation therapySettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungCell Line TumorGATA6 Transcription FactormedicineRetinoic acidAnimalsHumansLung cancerProtein Kinase InhibitorsWnt Signaling PathwayTranscription factorCell ProliferationMultidisciplinaryQRWnt signaling pathwayCell Differentiationmedicine.diseaseG1 Phase Cell Cycle CheckpointsXenograft Model Antitumor Assaysrespiratory tract diseasesErbB Receptorslung cancerAnimals; Carcinoma Non-Small-Cell Lung; Cell Differentiation; Cell Line Tumor; Cell Proliferation; Drug Resistance Neoplasm; ErbB Receptors; G1 Phase Cell Cycle Checkpoints; GATA6 Transcription Factor; Humans; Mice Nude; Protein Kinase Inhibitors; Signal Transduction; Tretinoin; Wnt Signaling Pathway; Xenograft Model Antitumor Assays030104 developmental biologychemistryDrug Resistance NeoplasmImmunologyCancer researchMedicineAdenocarcinomaEngineering sciences. TechnologyTyrosine kinaseSignal Transduction
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Cytoprotective and antioxidant properties of organic selenides for the myelin-forming cells, oligodendrocytes.

2018

Abstract Here a new series of twenty-one organoselenides, of potential protective activity, were synthesized and tested for their intrinsic cytotoxicity, anti-apoptotic and antioxidant capacities in oligodendrocytes. Most of the organoselenides were able to decrease the ROS levels, revealing antioxidant properties. Compounds 5b and 7b showed a high glutathione peroxidase (GPx)-like activities, which were 1.5 folds more active than ebselen. Remarkably, compound 5a diminished the formation of the oligodendrocytes SubG1 peak in a concentration-dependent manner, indicating its anti-apoptotic properties. Furthermore, based on the SwissADME web interface, we performed an in-silico structure-activ…

0301 basic medicineAntioxidantCell Survivalmedicine.medical_treatmentMolecular ConformationApoptosisCrystallography X-RayProtective Agents01 natural sciencesBiochemistryAntioxidantsCell Line03 medical and health scienceschemistry.chemical_compoundMyelinMiceStructure-Activity RelationshipOrganoselenium CompoundsDrug DiscoverymedicineAnimalsCytotoxicityMolecular Biologychemistry.chemical_classification010405 organic chemistryEbselenGlutathione peroxidaseOrganic ChemistryNeurodegenerationCells oligodendrocytesmedicine.diseaseG1 Phase Cell Cycle Checkpoints0104 chemical sciencesOligodendroglia030104 developmental biologymedicine.anatomical_structurechemistryBiochemistryApoptosisDrug DesignReactive Oxygen SpeciesBioorganic chemistry
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AMG900 as novel inhibitor of the translationally controlled tumor protein

2020

Abstract Introduction Cancer is one of the leading causes of death worldwide. Classical cytotoxic chemotherapy exerts high side effects and low tumor selectivity. Translationally controlled tumor protein (TCTP) is a target for differentiation therapy, a promising, new therapeutic approach, which is expected to be more selective and less toxic than cytotoxic chemotherapy. The aim of the present investigation was to identify novel TCTP inhibitors. Methods We performed in silico screening and molecular docking using a chemical library of more than 31,000 compounds to identify a novel inhibitor of TCTP. We tested AMG900 in vitro for binding to TCTP by microscale thermophoresis and co-immunoprec…

0301 basic medicineApoptosisCell Cycle ProteinsToxicologyResting Phase Cell CycleFlow cytometry03 medical and health sciences0302 clinical medicineCyclin D1Differentiation therapyCell Line TumorNeoplasmsTranslationally-controlled tumor proteinBiomarkers TumormedicineHumansCyclin D3medicine.diagnostic_testbiologyChemistryG1 PhaseTumor Protein Translationally-Controlled 1General MedicineMolecular Docking SimulationBlot030104 developmental biologyProtein Biosynthesis030220 oncology & carcinogenesisCancer cellMCF-7 CellsCancer researchbiology.proteinPhthalazinesCyclin-dependent kinase 6Chemico-Biological Interactions
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Cyclin-Dependent Kinase 4 Regulates Adult Neural Stem Cell Proliferation and Differentiation in Response to Insulin

2017

Abstract Insulin is one of the standard components used to culture primary neurospheres. Although it stimulates growth of different types of cells, the effects of insulin on adult neural stem cells (NSCs) have not been well characterized. Here, we reveal that insulin stimulates proliferation, but not survival or self-renewal, of adult NSCs. This effect is mediated by insulin receptor substrate 2 (IRS2) and subsequent activation of the protein kinase B (or Akt), leading to increased activity of the G1-phase cyclin-dependent kinase 4 (Cdk4) and cell cycle progression. Neurospheres isolated from Irs2-deficient mice are reduced in size and fail to expand in culture and this impaired proliferati…

0301 basic medicineInsulin Receptor Substrate ProteinsNeurogenesisCellular differentiationBiologyAdult neurogenesisMice03 medical and health sciencesNeural Stem CellsCyclin-dependent kinaseNeurosphereAnimalsInsulinPhosphorylationNeuritogenesisProtein kinase BCell ProliferationCell CycleG1 PhaseCyclin-dependent kinaseCyclin-Dependent Kinase 4Cell DifferentiationCell BiologyIRS2Neural stem cellCell biology030104 developmental biologyVentricular-subventricular zoneInsulin Receptor Substrate Proteinsbiology.proteinMolecular MedicineNeurospheresbiological phenomena cell phenomena and immunityStem cellDevelopmental BiologyStem Cells
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Unusual roles of caspase-8 in triple-negative breast cancer cell line MDA-MB-231

2015

Triple-negative breast cancer (TNBC) is a clinically aggressive form of breast cancer that is unresponsive to endocrine agents or trastuzumab. TNBC accounts for ~10-20% of all breast cancer cases and represents the form with the poorest prognosis. Patients with TNBC are at higher risk of early recurrence, mainly in the lungs, brain and soft tissue, therefore, there is an urgent need for new therapies. The present study was carried out in MDA-MB-231 cells, where we assessed the role of caspase-8 (casp-8), a critical effector of death receptors, also involved in non‑apoptotic functions. Analysis of casp-8 mRNA and protein levels indicated that they were up-regulated with respect to the normal…

0301 basic medicineMDA-MB-231 cellCancer ResearchDown-RegulationTriple Negative Breast NeoplasmsTransfectionResting Phase Cell Cycle03 medical and health sciencesKruppel-Like Factor 40302 clinical medicineHMGA2Breast cancerCell Line TumormedicineHumansRNA Small InterferingCaspase-8 unusual roleTriple-negative breast cancerCaspase 8Triple-negative breast cancer cellbiologyOncogeneCaspase-8 knockdownCell CycleG1 PhaseCancerCell cyclemedicine.diseaseMolecular medicineKLF4Invasivity and metastasi030104 developmental biologyOncologyKLF4030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleCell cycle regulator
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Artesunate Impairs Growth in Cisplatin-Resistant Bladder Cancer Cells by Cell Cycle Arrest, Apoptosis and Autophagy Induction

2020

Cisplatin, which induces DNA damage, is standard chemotherapy for advanced bladder cancer (BCa). However, efficacy is limited due to resistance development. Since artesunate (ART), a derivative of artemisinin originating from Traditional Chinese Medicine, has been shown to exhibit anti-tumor activity, and to inhibit DNA damage repair, the impact of artesunate on cisplatin-resistant BCa was evaluated. Cisplatin-sensitive (parental) and cisplatin-resistant BCa cells, RT4, RT112, T24, and TCCSup, were treated with ART (1&ndash

0301 basic medicineautophagyRMCell cycle checkpointDNA RepairDNA damageArtesunateCell Cycle ProteinsArticlegrowth inhibition03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumormedicineHumansddc:610Medicine Chinese Traditionalskin and connective tissue diseaseslcsh:QH301-705.5Cell ProliferationCisplatinartesunate (ART)Cell growthAutophagyapoptosisGeneral MedicineCell cycleG1 Phase Cell Cycle Checkpoints030104 developmental biologychemistrylcsh:Biology (General)Urinary Bladder NeoplasmsApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchbladder cancer (BCa)Growth inhibitioncisplatin resistanceMicrotubule-Associated Proteinsmedicine.drug
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Synthesis, antiproliferative activity and possible mechanism of action of novel 2-acetamidobenzamides bearing the 2-phenoxy functionality.

2015

Several new 2-(2-phenoxyacetamido)benzamides 17a-v, 21 and 22 were synthesized by stirring in pyridine the acid chlorides 16a-e and the appropriate5-R-4-R1-2-aminobenzamide 15a-e and initially evaluated in vitro for antiproliferative activity against the K562 (human chronic myelogenous leukemia) cell line. Some of synthesized compounds were evaluated for their in vitro antiproliferative activity against the full NCI tumor cell line panel derived from nine clinically isolated cancer types (leukemia, non-small cell lung, colon, CNS, melanoma, ovarian, renal, prostate and breast). The most active compounds caused an arrest of K562 cells in the G0-G1 phase of cell cycle and induction of apoptos…

3003Clinical BiochemistryCellPharmaceutical ScienceAntineoplastic AgentsApoptosisAntiproliferative activityPharmacologyG0/G1 arrestBiochemistryArticle2-(2-Phenoxyacetamido)benzamideAntineoplastic AgentStructure-Activity RelationshipBenzamideSettore BIO/10 - BiochimicaCell Line TumorDrug DiscoveryG1 Phase Cell Cycle CheckpointK562 CellmedicineHumansMolecular BiologyCell ProliferationCell growthChemistryDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryApoptosiCell cyclemedicine.diseaseCaspaseSettore CHIM/08 - Chimica FarmaceuticaG1 Phase Cell Cycle CheckpointsLeukemiamedicine.anatomical_structureMicroscopy FluorescenceCell cultureApoptosisCaspasesBenzamidesMolecular MedicineDrug Screening Assays AntitumorK562 CellsPro-caspase 3HumanK562 cellsChronic myelogenous leukemiaBioorganicmedicinal chemistry
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Knockdown of NANOG Reduces Cell Proliferation and Induces G0/G1 Cell Cycle Arrest in Human Adipose Stem Cells

2019

The core components of regenerative medicine are stem cells with high self-renewal and tissue regeneration potentials. Adult stem cells can be obtained from many organs and tissues. NANOG, SOX2 and OCT4 represent the core regulatory network that suppresses differentiation-associated genes, maintaining the pluripotency of mesenchymal stem cells. The roles of NANOG in maintaining self-renewal and undifferentiated status of adult stem cells are still not perfectly established. In this study we define the effects of downregulation of NANOG in maintaining self-renewal and undifferentiated state in mesenchymal stem cells (MSCs) derived from subcutaneous adipose tissue (hASCs). hASCs were expanded…

AdultHomeobox protein NANOGDown-RegulationBiologyArticleCatalysisSettore MED/13 - Endocrinologialcsh:ChemistryInorganic ChemistrySOX2human adipose stem cellHumansCell Self RenewalPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyCells CulturedSpectroscopyCell Proliferationmolecular_biologyCell growthOrganic ChemistryMesenchymal stem cellDNMT1lentiviral transductionCell DifferentiationMesenchymal Stem CellsNanog Homeobox ProteinGeneral MedicineMiddle AgedCell cycleG1 Phase Cell Cycle CheckpointsComputer Science ApplicationsCell biologySettore MED/18 - Chirurgia GeneraleNANOGlcsh:Biology (General)lcsh:QD1-999Gene Knockdown Techniquesembryonic structures<i>NANOG</i>Female<i>DNMT1</i>CDKN1Bbiological phenomena cell phenomena and immunityStem cellcell cycle regulationAdult stem cell
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Toward a Rational Design of Polyamine-Based Zinc-Chelating Agents for Cancer Therapies.

2020

In vitro viability assays against a representative panel of human cancer cell lines revealed that polyamines L1a and L5a displayed remarkable activity with IC50 values in the micromolar range. Preliminary research indicated that both compounds promoted G1 cell cycle arrest followed by cellular senescence and apoptosis. The induction of apoptotic cell death involved loss of mitochondrial outer membrane permeability and activation of caspases 3/7. Interestingly, L1a and L5a failed to activate cellular DNA damage response. The high intracellular zinc-chelating capacity of both compounds, deduced from the metal-specific Zinquin assay and ZnL2+ stability constant values in solution, strongly sup…

Antineoplastic AgentsApoptosis01 natural sciences03 medical and health scienceschemistry.chemical_compoundStructure-Activity RelationshipCell Line TumorDrug DiscoveryPolyaminesHumansCytotoxicityCaspase030304 developmental biologyChelating Agents0303 health sciencesbiologyMolecular StructureChemistryRational designG1 Phase Cell Cycle Checkpoints0104 chemical sciencesCell biology010404 medicinal & biomolecular chemistryZincModels ChemicalApoptosisCell cultureDrug Designbiology.proteinMolecular MedicineQuantum TheoryDrug Screening Assays AntitumorPolyamineG1 phaseIntracellularJournal of medicinal chemistry
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TORC1 controls G1–S cell cycle transition in yeast via Mpk1 and the greatwall kinase pathway

2015

The target of rapamycin complex 1 (TORC1) pathway couples nutrient, energy and hormonal signals with eukaryotic cell growth and division. In yeast, TORC1 coordinates growth with G1–S cell cycle progression, also coined as START, by favouring the expression of G1 cyclins that activate cyclin-dependent protein kinases (CDKs) and by destabilizing the CDK inhibitor Sic1. Following TORC1 downregulation by rapamycin treatment or nutrient limitation, clearance of G1 cyclins and C-terminal phosphorylation of Sic1 by unknown protein kinases are both required for Sic1 to escape ubiquitin-dependent proteolysis prompted by its flagging via the SCFCdc4 (Skp1/Cul1/F-box protein) ubiquitin ligase complex.…

BioquímicaBiologiaSaccharomyces cerevisiae ProteinsImmunoblottingGeneral Physics and AstronomyCell Cycle ProteinsSaccharomyces cerevisiaeMechanistic Target of Rapamycin Complex 1ArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineCyclin-dependent kinaseCyclinsImmunoprecipitationProtein Phosphatase 2Cell division control protein 4PhosphorylationProtein kinase ACyclin-Dependent Kinase Inhibitor Proteins030304 developmental biology0303 health sciencesMultidisciplinarybiologyTOR Serine-Threonine KinasesUbiquitin-Protein Ligase ComplexesGeneral ChemistryBlotting NorthernFlow CytometryG1 Phase Cell Cycle CheckpointsSic1Cyclin-Dependent KinasesCell biologyBiochemistryMultiprotein Complexes030220 oncology & carcinogenesisUbiquitin ligase complexbiology.proteinIntercellular Signaling Peptides and ProteinsPhosphorylationTOR Serine-Threonine KinasesMitogen-Activated Protein KinasesPeptidesProtein KinasesCyclin-dependent kinase inhibitor proteinNature Communications
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