Search results for "Cyclin D3"

showing 4 items of 4 documents

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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Differences in the mechanisms of growth control in contact-inhibited and serum-deprived human fibroblasts

1997

In the present work we studied mechanisms of growth control in contact-inhibited and serum-deprived human diploid fibroblasts. The observation that the effects on [3H]thymidine incorporation and reduction of retinoblastoma gene product-phosphorylation were additive when contact-inhibition and serum-deprivation were combined led us to the conclusion that the underlying mechanisms might be different. Both contact-inhibition and serum-deprivation led to a strong decrease of cdk4-kinase-activity and cdk2-phosphorylation at Thr 160, while the total amounts of cdk4 and cdk2 remained constant. In contact-inhibited cells, we revealed a strong protein accumulation of the cdk2-inhibitor p27 and a sli…

Cancer ResearchCell Cycle ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinCulture Media Serum-FreeS PhaseCyclin D1CyclinsProto-Oncogene ProteinsCDC2-CDC28 KinasesGeneticsmedicineHumansCyclin D1Cyclin D3PhosphorylationCyclin D3FibroblastMolecular BiologyCyclin-Dependent Kinase Inhibitor p16CyclinbiologyCell growthTumor Suppressor ProteinsCyclin-Dependent Kinase 2Cyclin-dependent kinase 2G1 PhaseCyclin-Dependent Kinase 4FibroblastsDiploidyCyclin-Dependent KinasesCulture MediaCell biologymedicine.anatomical_structureCell culturebiology.proteinbiological phenomena cell phenomena and immunitySignal transductionMicrotubule-Associated ProteinsCell DivisionCyclin-Dependent Kinase Inhibitor p27Oncogene
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Deregulation of the G1 to S-phase cell cycle checkpoint is involved in the pathogenesis of human osteosarcoma.

2004

Osteosarcoma (OS) displays complex karyotypes with numerical changes as well as structural abnormalities suggesting that several oncogenes and tumor suppressor genes may be implicated in the biology of OS. The aim of our study was to investigate the possible implication of the molecular alterations of the G1 to S-phase checkpoint genes in the pathogenesis of OS. We analyzed samples from 29 patients and found molecular alterations of the RB and TP53 genes in 6 (21%) and 3 (10%) cases, respectively. Homozygous deletion of the INK4A/ARF locus and methylation of INK4A was detected in 3 (10%) and 2 (7%) cases, respectively. CDK4 and MDM2 co-amplification was observed in 1 case (3%). Cyclin D3 is…

MaleCell cycle checkpointAdolescentLocus (genetics)Bone NeoplasmsBiologyPathology and Forensic MedicineS PhasePathogenesisGene duplicationmedicineHumansCHEK1Cyclin D3ChildMolecular BiologyAgedOsteosarcomaReverse Transcriptase Polymerase Chain ReactionCell CycleAge FactorsG1 PhaseGene AmplificationCell BiologyG2-M DNA damage checkpointMiddle Agedmedicine.diseaseGenes cdcHistory 16th CenturyCancer researchOsteosarcomaFemaleChromosomes Human Pair 9Diagnostic molecular pathology : the American journal of surgical pathology, part B
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Cucurbitacins as inducers of cell death and a rich source of potential anticancer compounds.

2011

Triterpenes have been reported to induce cell death. One relevant group of this family of compounds is cucurbitacins, which have been studied as inducers of apoptosis in various cancer cell lines. The most significant mechanisms with regard to the apoptotic effects of cucurbitacins are their ability to modify transcriptional activities via nuclear factors or genes and their capability to activate or inhibit pro- or anti-apoptotic proteins. Still, while the majority of studies on these compounds have dealt with their apoptotic effects on cancer cell lines, several research groups have also explored their anti-inflammatory activities. In general, cucurbitacins are considered to be selective i…

PharmacologyMAPK/ERK pathwayProgrammed cell deathCell CycleApoptosisCucurbitacinsCell cycleBiologyAntineoplastic Agents PhytogenicstatCell biologyCucurbitacinsApoptosisDrug Discoverybiology.proteinAnimalsHumansCyclin D3STAT3Signal TransductionCurrent pharmaceutical design
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