Search results for "Cell cycle checkpoint"

showing 10 items of 126 documents

Class I histone deacetylases regulate p53/NF-κB crosstalk in cancer cells

2016

The transcription factors NF-κB and p53 as well as their crosstalk determine the fate of tumor cells upon therapeutic interventions. Replicative stress and cytokines promote signaling cascades that lead to the co-regulation of p53 and NF-κB. Consequently, nuclear p53/NF-κB signaling complexes activate NF-κB-dependent survival genes. The 18 histone deacetylases (HDACs) are epigenetic modulators that fall into four classes (I-IV). Inhibitors of histone deacetylases (HDACi) become increasingly appreciated as anti-cancer agents. Based on their effects on p53 and NF-κB, we addressed whether clinically relevant HDACi affect the NF-κB/p53 crosstalk. The chemotherapeutics hydroxyurea, etoposide, an…

0301 basic medicineDNA damageApoptosisModels BiologicalHistone Deacetylases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorNeoplasmsHumansHydroxyureaEpigeneticsTranscription factorCellular SenescenceEtoposidebiologyNF-kappa BNF-κBCell Cycle CheckpointsDNA NeoplasmCell BiologyHDAC6Gene Expression Regulation NeoplasticHistone Deacetylase InhibitorsCrosstalk (biology)030104 developmental biologyHistonechemistry030220 oncology & carcinogenesisMutationCancer cellbiology.proteinCancer researchTumor Suppressor Protein p53VidarabineDNA DamageSignal TransductionCellular Signalling
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DHA induces Jurkat T-cell arrest in G2/M phase of cell cycle and modulates the plasma membrane expression of TRPC3/6 channels.

2021

Abstract We investigated whether docosahexaenoic acid (DHA), a dietary n-3 fatty acid, modulates calcium (Ca2+) signaling and cell cycle progression in human Jurkat T-cells. Our study demonstrates that DHA inhibited Jurkat T-cell cycle progression by blocking their passage from S phase to G2/M phase. In addition, DHA decreased the plasma membrane expression of TRPC3 and TRPC6 calcium channels during T-cell proliferation. Interestingly, this fatty acid increased plasma membrane expression of TRPC6 after 24 h of mitogenic stimulation by phorbol-13-myristate-12-acetate (PMA) and ionomycin. These variations in the membrane expression of TRPC3 and TRPC6 channels were not directly correlated with…

0301 basic medicineDocosahexaenoic AcidsT-Lymphocyteschemistry.chemical_elementCalciumBiochemistryJurkat cellsCalcium in biology03 medical and health scienceschemistry.chemical_compoundJurkat CellsTRPC3TRPC6 Cation ChannelHumansTRPC Cation Channels030102 biochemistry & molecular biologyVoltage-dependent calcium channelIonomycinCell MembraneGeneral MedicineCell cycleCell biologyG2 Phase Cell Cycle Checkpoints030104 developmental biologychemistryGene Expression RegulationDocosahexaenoic acidIonomycinM Phase Cell Cycle CheckpointsTetradecanoylphorbol AcetateBiochimie
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Anthranilamide-based 2-phenylcyclopropane-1-carboxamides, 1,1'-biphenyl-4-carboxamides and 1,1'-biphenyl-2-carboxamides: Synthesis biological evaluat…

2017

Abstract Several anthranilamide-based 2-phenylcyclopropane-1-carboxamides 13a-f, 1,1’-biphenyl-4-carboxamides 14a-f and 1,1’-biphenyl-2-carboxamides 17a-f were obtained by a multistep procedure starting from the (1S,2S)-2-phenylcyclopropane-1-carbonyl chloride 11, the 1,1'-biphenyl-4-carbonyl chloride 12 or the 1,1'-biphenyl-2-carbonyl chloride 16 with the appropriate anthranilamide derivative 10a-f. Derivatives 13a-f, 14a-f and 17a-f showed antiproliferative activity against human leukemia K562 cells. Among these derivatives 13b, 14b and 17b exerted a particular cytotoxic effect on tumor cells. Derivative 17b showed a better antitumoral effect on K562 cells than 13b and 14b. Analyses perfo…

0301 basic medicineG2 Phase2-Phenylcyclopropane-1-carboxamides 11’-biphenyl-4-carboxamides 11’-biphenyl-2-carboxamides G2/M arrest Phospho-ATM and gH2AX increaseDNA RepairDNA repairStereochemistryAntineoplastic AgentsApoptosisChloride03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaDrug DiscoverymedicineCytotoxic T cellHumansortho-AminobenzoatesMode of actionCell ProliferationPharmacologyChemistryOrganic ChemistryGeneral MedicineCell Cycle CheckpointsCell cycleSettore CHIM/08 - Chimica Farmaceutica030104 developmental biologyMechanism of actionApoptosis030220 oncology & carcinogenesismedicine.symptomK562 CellsDNAmedicine.drugDNA Damage
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Understanding the implication of autophagy in the activation of hepatic stellate cells in liver fibrosis: are we there yet?

2021

Liver fibrosis (LF) occurs as a result of persistent liver injury and can be defined as a pathologic, chronic, wound-healing process in which functional parenchyma is progressively replaced by fibrotic tissue. As a phenomenon involved in the majority of chronic liver diseases, and therefore prevalent, it exerts a significant impact on public health. This impact becomes even more patent given the lack of a specific pharmacological therapy, with LF only being ameliorated or prevented through the use of agents that alleviate the underlying causes. Hepatic stellate cells (HSCs) are fundamental mediators of LF, which, activated in response to pro-fibrotic stimuli, transdifferentiate from a quies…

0301 basic medicineLiver injuryLiver CirrhosisProgrammed cell deathCell cycle checkpointbusiness.industryAutophagymedicine.diseasePathology and Forensic Medicine03 medical and health sciences030104 developmental biology0302 clinical medicineCell culture030220 oncology & carcinogenesisLipid dropletCancer researchHepatic stellate cellmedicineAutophagyHepatic Stellate CellsAnimalsHumansbusinessMyofibroblastThe Journal of pathologyReferences
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Cytotoxicity ofSalvia miltiorrhizaAgainst Multidrug-Resistant Cancer Cells

2016

Salvia miltiorrhiza Bunge (Lamiaceae) is a well-known Chinese herb that possesses numerous therapeutic activities, including anticancer effects. In this study, the cytotoxicity and the biological mechanisms of S. miltiorrhiza (SM) root extract on diverse resistant and sensitive cancer cell lines were investigated. CEM/ADR5000 cells were 1.68-fold resistant to CCRF-CEM cells, while HCT116 (p53[Formula: see text] and U87.MG[Formula: see text]EGFR cells were hypersensitive (collateral sensitive) compared to their parental cells. SM root extract stimulated ROS generation, cell cycle S phase arrest and apoptosis. The induction of the intrinsic apoptotic pathway was validated by increased cleavag…

0301 basic medicinePoly ADP ribose polymerasep38 mitogen-activated protein kinasesApoptosisSalvia miltiorrhizaCaspase 3PharmacologyBiologySalvia miltiorrhiza03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsHumansCytotoxicityCell Cycle CheckpointsGeneral MedicineCell cycleAntineoplastic Agents PhytogenicMolecular biology030104 developmental biologyComplementary and alternative medicineDrug Resistance NeoplasmApoptosisCaspases030220 oncology & carcinogenesisCancer cellReactive Oxygen SpeciesDrugs Chinese HerbalThe American Journal of Chinese Medicine
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Dibutyltin(IV) and Tributyltin(IV) Derivatives of meso-Tetra(4 sulfonatophenyl)porphine Inhibit the Growth and the Migration of Human Melanoma Cells.

2019

Melanoma is the most aggressive and deadly form of skin cancer, which is largely due to its propensity to metastasize. Therefore, with the aim to inhibit the growth and the metastatic dissemination of melanoma cells and to provide a novel treatment option, we studied the effects of the melanoma treatment with two organotin(IV) complexes of the meso-tetra(4-sulfonato-phenyl)porphine, namely (Bu2Sn)2TPPS and (Bu3Sn)4TPPS. In particular, we showed that nanomolar concentrations of (Bu2Sn)2TPPS and (Bu3Sn)4TPPS are sufficient to inhibit melanoma cell growth, to increase the expression of the full-length poly (ADP-ribose) polymerase (PARP-1), to induce the cell cycle arrest respectively at G2/M a…

0301 basic medicinePorphyrinsCellAntineoplastic AgentsApoptosisorganotin(IV)migrationArticleBRAF03 medical and health sciences0302 clinical medicineCyclin D1Cell MovementCell Line Tumormelanoma; organotin(IV); cellular growth; BRAF; cell cycle; migrationmedicinemelanomaHumansSTAT3Cell ProliferationDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryMelanomaCell migrationCell Cycle CheckpointsGeneral Medicinecellular growthCell cyclemedicine.disease030104 developmental biologymedicine.anatomical_structureFocal Adhesion Kinase 1030220 oncology & carcinogenesisbiology.proteinCancer researchcell cycleSkin cancerSignal Transduction
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Pekinenin E Inhibits the Growth of Hepatocellular Carcinoma by Promoting Endoplasmic Reticulum Stress Mediated Cell Death.

2017

Hepatocellular carcinoma (HCC) is a malignant primary liver cancer with poor prognosis. In the present study, we report that pekinenin E (PE), a casbane diterpenoid derived from the roots of Euphorbia pekinensis, has a strong antitumor activity against human HCC cells both in vitro and in vivo. PE suppressed the growth of human HCC cells Hep G2 and SMMC-7721. In addition, PE-mediated endoplasmic reticulum (ER) stress caused increasing expressions of C/EBP homologous protein (CHOP), leading to apoptosis in HCC cells both in vitro and in vivo. Inhibition of ER stress with CHOP small interfering RNA or 4-phenyl-butyric acid partially reversed PE-induced cell death. Furthermore, PE induced S ce…

0301 basic medicineProgrammed cell deathSmall interfering RNAPathologymedicine.medical_specialtyCell cycle checkpointCHOP03 medical and health sciencesmedicinePharmacology (medical)Original ResearchPharmacologybusiness.industryEndoplasmic reticulumlcsh:RM1-950apoptosisdigestive system diseasesHep G2030104 developmental biologylcsh:Therapeutics. PharmacologyApoptosishepatocarcinomacell cycle arrestUnfolded protein responseCancer researchbusinessER stresspekinenin EFrontiers in pharmacology
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Sicilian Litchi Fruit Extracts Induce Autophagy versus Apoptosis Switch in Human Colon Cancer Cells

2018

Litchi chinensis Sonnerat is a tropical tree whose fruits contain significant amounts of bioactive polyphenols. Litchi cultivation has recently spread in Sicily where the climate conditions are particularly favorable for this crop. Recent findings have shown that Litchi extracts display anti-tumor and pro-apoptotic effects in vitro, but the precise underlying mechanisms have not been fully elucidated. In this study, we report for the first time the effects of Sicilian litchi fruit extracts on colon cancer cells. The results indicated that litchi exocarp, mesocarp and endocarp fractions reduce the viability and clonogenic growth of HT29 cells. These effects were due to cell cycle arrest in t…

0301 basic medicineProgrammed cell deathautophagyCell cycle checkpointAtg1Apoptosislcsh:TX341-641Litchi chinensisArticle03 medical and health sciencesHT29 Cells0302 clinical medicineLitchiSettore BIO/10 - BiochimicaHumansClonogenic assaySicilyNutrition and DieteticsPlant ExtractsChemistryKinaseAutophagyPolyphenolsLitchi chinensiCell Cycle CheckpointsAntineoplastic Agents PhytogenicCell biology030104 developmental biologycolon cancerApoptosisFruit030220 oncology & carcinogenesisColonic Neoplasmsanti-tumor activityCaco-2 Cells<i>Litchi chinensis</i>HT29 Cellslcsh:Nutrition. Foods and food supplyPhytotherapySignal TransductionFood ScienceNutrients
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Whi7 is an unstable cell-cycle repressor of the Start transcriptional program

2017

Start is the main decision point in eukaryotic cell cycle in which cells commit to a new round of cell division. It involves the irreversible activation of a transcriptional program by G1 CDK-cyclin complexes through the inactivation of Start transcriptional repressors, Whi5 in yeast or Rb in mammals. Here we provide novel keys of how Whi7, a protein related at sequence level to Whi5, represses Start. Whi7 is an unstable protein, degraded by the SCFGrr1 ubiquitin-ligase, whose stability is cell cycle regulated by CDK1 phosphorylation. Importantly, Whi7 associates to G1/S gene promoters in late G1 acting as a repressor of SBF-dependent transcription. Our results demonstrate that Whi7 is a ge…

0301 basic medicineSaccharomyces cerevisiae ProteinsTranscription GeneticCell divisionScienceGeneral Physics and AstronomyRepressorSaccharomyces cerevisiaeBiologyArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCyclinsGene Expression Regulation Fungallcsh:ScienceGeneticsRegulation of gene expressionCyclin-dependent kinase 1MultidisciplinaryYY1QPromoterCell Cycle CheckpointsGeneral ChemistryCell cycleRepressor Proteins030104 developmental biologyGATAD2Blcsh:QNature Communications
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Cytotoxicity of seven naturally occurring phenolic compounds towards multi-factorial drug-resistant cancer cells

2016

Abstract Introduction In medical oncology, multi-drug resistance (MDR) of cancer cells continues to be a major impediment. We are in quest of novel anti-proliferative agents to overcome drug-resistant tumor cells. Methods In the present study, we investigated the cytotoxicity of 7 naturally occurring phenolic compounds including two isoflavonoids alpinumisoflavone ( 1 ) and laburnetin ( 2 ), one biflavonoid amentoflavone ( 3) , three lignans pycnanthulignene A ( 4 ), pycnanthulignene B ( 5 ), and syringaresinol ( 7 ) and one xanthone, euxanthone ( 6 ) against 9 drug-sensitive and MDR cancer cell lines. The resazurin reduction assay was used to evaluate the cytotoxicity of these compounds, w…

0301 basic medicineSyringaresinolPharmaceutical SciencePharmacologyAmentoflavone03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhenolsIsoflavonoidCell Line TumorNeoplasmsOxazinesDrug DiscoveryHumansCytotoxic T cellCytotoxicityMembrane Potential MitochondrialPharmacologyCell Cycle CheckpointsAlpinumisoflavoneAntineoplastic Agents PhytogenicDrug Resistance MultipleEnzyme Activation030104 developmental biologyXanthenesComplementary and alternative medicinechemistryDrug Resistance NeoplasmApoptosisCaspases030220 oncology & carcinogenesisCancer cellMolecular MedicineReactive Oxygen SpeciesPhytomedicine
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