Search results for "Cell growth"

showing 10 items of 662 documents

Heat Shock Protein 60 in Cardiovascular Physiology and Diseases.

2020

Heat shock protein 60 (HSP60) is a highly conserved protein abundantly expressed in both prokaryotic and eukaryotic cells. In mammals, HSP60 has been primarily considered to reside in the mitochondria, where HSP60 and HSP10 form a complex and facilitate mitochondrial protein folding. However, HSP60 is also observed in the cytoplasm, the plasma membrane, and the extracellular space. HSP60 regulates a broad spectrum of cellular events including protein trafficking, peptide hormone signaling, cell survival, cell proliferation, inflammation, and immunization. In the cardiovascular system, growing evidence indicates that HSP60 could not only play an important role under physiological conditions,…

0301 basic medicineanimal structuresMini Reviewheat shock proteinheart failureInflammationchemical and pharmacologic phenomenacardiomyocyteBiologyMitochondrionBiochemistry Genetics and Molecular Biology (miscellaneous)Biochemistrycomplex mixtures03 medical and health sciences0302 clinical medicineHeat shock proteinmedicineMolecular Bioscienceslcsh:QH301-705.5Molecular BiologyCell growthfungiCardiovascular physiologyCell biology030104 developmental biologylcsh:Biology (General)Cytoplasm030220 oncology & carcinogenesisHSP60medicine.symptomSignal transductionatherosclerosisHSP60Frontiers in molecular biosciences
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Effects of Pimozide Derivatives on pSTAT5 in K562 Cells

2017

STAT5 is a transcription factor, a member of the STAT family of signaling proteins. STAT5 is involved in many types of cancer, including chronic myelogenous leukemia (CML), in which this protein is found constitutively activated as a consequence of BCR-ABL expression. The neuroleptic drug pimozide was recently reported to act as an inhibitor of STAT5 phosphorylation and is capable of inducing apoptosis in CML cells in vitro. Our research group has synthesized simple derivatives of pimozide with cytotoxic activity and that are able to decrease the levels of phosphorylated STAT5. In this work we continued the search for novel STAT5 inhibitors, synthesizing compounds in which the benzoimidazol…

0301 basic medicineantiproliferationApoptosisPharmacologyBiochemistryAntineoplastic Agent0302 clinical medicinePimozidehemic and lymphatic diseasesDrug DiscoverySTAT5 Transcription FactorCytotoxic T cellPhosphorylationGeneral Pharmacology Toxicology and PharmaceuticsBCR-ABL-expressing leukemia; STAT5 inhibitors; antiproliferation; apoptosis; pimozideSTAT5Molecular StructurebiologyPimozidefood and beverages030220 oncology & carcinogenesisMolecular MedicinePhosphorylationHumanmedicine.drugAntineoplastic AgentsNOStructure-Activity Relationship03 medical and health sciencesK562 CellmedicineHumansTranscription factorCell ProliferationPharmacologyDose-Response Relationship DrugCell growthSTAT5 inhibitorsOrganic ChemistryApoptosiSTAT5 inhibitormedicine.disease030104 developmental biologyPharmacology Toxicology and Pharmaceutics (all)biology.proteinCancer researchBCR-ABL-expressing leukemiaDrug Screening Assays AntitumorK562 CellsK562 cellsChronic myelogenous leukemiaChemMedChem
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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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Effect of Manganese Chloride and of Cotreatment with Cadmium Chloride on the In Vitro Proliferative, Motile, and Invasive Behavior of MDA-MB231 Breas…

2019

We examined the dose&ndash

0301 basic medicinecadmiumproliferationPharmaceutical ScienceBreast NeoplasmsCadmium chloridemedicine.disease_causeArticleAnalytical ChemistryMetastasislcsh:QD241-44103 medical and health scienceschemistry.chemical_compound0302 clinical medicineBreast cancerCadmium ChlorideChlorideslcsh:Organic chemistryCell Movementbreast cancer cellCell Line TumorDrug DiscoverymedicineHumansSettore BIO/06 - Anatomia Comparata E CitologiaPhysical and Theoretical ChemistrychemotaxisCell ProliferationCell growthOrganic Chemistrymedicine.diseasechemoinvasionIn vitroEpithelium030104 developmental biologymedicine.anatomical_structureManganese CompoundschemistryChemistry (miscellaneous)030220 oncology & carcinogenesisCancer cellCancer researchmanganeseMolecular MedicineFemalechemotaxiCarcinogenesisbreast cancer cellsMolecules
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Loss of MCL1 function sensitizes the MDA-MB-231 breast cancer cells to rh-TRAIL by increasing DR4 levels.

2019

Triple-negative breast cancer (TNBC) is a form of BC characterized by high aggressiveness and therapy resistance probably determined by cancer stem cells. MCL1 is an antiapoptotic Bcl-2 family member that could limit the efficacy of anticancer agents as recombinant human tumor necrosis factor related apoptosis-inducing ligand (rh-TRAIL). Here, we investigated MCL1 expression in TNBC tissues and cells. We found MCL1 differentially expressed (upregulated or downregulated) in TNBC tissues. Furthermore, in comparison to the human mammary epithelial cells, we found that MDA-MB-231 cells show similar messenger RNA levels but higher MCL1 protein levels, whereas it resulted downregulated in MDA-MB-…

0301 basic medicinecancer stem cellIndolesPhysiologyCell SurvivalClinical BiochemistryCellPopulationApoptosisTNF-Related Apoptosis-Inducing Ligand03 medical and health sciences0302 clinical medicineCancer stem cellSettore BIO/10 - BiochimicaCell Line Tumormedicinerh-TRAILBiomarkers TumorGene silencingHumansViability assayGene SilencingeducationCell ShapeCell ProliferationMembrane Potential Mitochondrialeducation.field_of_studySulfonamidesChemistryCell growthCell CycleCell BiologyCell cycleRecombinant ProteinsGene Expression Regulation NeoplasticReceptors TNF-Related Apoptosis-Inducing Ligand030104 developmental biologymedicine.anatomical_structureMCL1ApoptosisDR4 receptor030220 oncology & carcinogenesisCancer researchtriple-negative breast cancerMyeloid Cell Leukemia Sequence 1 ProteinJournal of cellular physiology
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An Ethanolic Extract of Ampelopsis Radix Exerts Anti-colorectal Cancer Effects and Potently Inhibits STAT3 Signaling In Vitro

2017

Colorectal cancer (CRC) is a leading cause of cancer-related morbidity and mortality worldwide. Signal transducer and activator of transcription 3 (STAT3) signaling is constantly activated in CRC, and has been proposed as a pathogenic factor and a therapeutic target of CRC. Ampelopsis Radix (AR), a traditional Chinese medicinal herb, possesses low toxicity and has long been used clinically for the treatment of cancers including CRC. Some constituents of AR have been reported to exert anticancer properties by targeting STAT3. However, the anti-CRC mode and mechanism of action of AR have not been fully elucidated. Here, we investigated the involvement of STAT3 signaling in the anti-CRC effect…

0301 basic medicinecolorectal cancerBiologyPharmacologymigrationSTAT303 medical and health sciences0302 clinical medicinemedicineCytotoxic T cellPharmacology (medical)STAT3neoplasmsOriginal ResearchPharmacologyCell growthlcsh:RM1-950apoptosisCell migrationAmpelopsis Radixinvasiondigestive system diseaseslcsh:Therapeutics. Pharmacology030104 developmental biologyMechanism of actionApoptosis030220 oncology & carcinogenesisSTAT proteinbiology.proteinPhosphorylationmedicine.symptomFrontiers in Pharmacology
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Polyphosphate Reverses the Toxicity of the Quasi-Enzyme Bleomycin on Alveolar Endothelial Lung Cells In Vitro

2021

Simple Summary Bleomycin (BLM) is a medication introduced used to treat various types of cancer, including testicular cancer, ovarian cancer, and Hodgkin’s disease. Its most serious side effect is pulmonary fibrosis and impaired lung function. Using A549 human lung cells it is shown that, in parallel to an increased cell toxicity and DNA damage, BLM causes a marked enlargement of the cell nucleus. This effect is abolished by inorganic polyphosphate (polyP), if this physiological polymer is administered together with BLM. The detoxification of BLM is–most likely–caused by the upregulation of the gene encoding the BLM hydrolase which inactivates BLM in vitro and in vivo. This study contribute…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA damageBleomycinlcsh:RC254-282Article03 medical and health scienceschemistry.chemical_compound0302 clinical medicineanti-SARS-CoV-2 activityDownregulation and upregulationprevention of fibrosischemistry.chemical_classificationbleomycinpulmonary fibrosisurogenital systemChemistryCell growthCOVID-19nutritional and metabolic diseasespolyphosphatelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologyIn vitroChromatin030104 developmental biologyEnzymeOncology030220 oncology & carcinogenesisToxicityCancers
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Bisphenolic compounds alter gene expression in MCF-7 cells through interaction with estrogen receptor α

2020

Plasticizers released from microplastic are increasingly viewed with concern. While adverse health effects induced by bisphenol A and its analogues on marine animals are well documented in the literature, the endocrine potential of bisphenolic compounds on human health remains elusive. We applied next generation sequencing (NGS) with the estrogen receptor α (ERα) positive human breast cancer cell line MCF-7 treated with 17-β-estradiol (E2), bisphenol A (BPA), bisphenol B (BPB), bisphenol Z (BPZ) and tetramethyl bisphenol A (4MeBPA). We used molecular docking, microscale thermophoresis, ERα activation assay, and cell cycle experiments on MCF-7 and ERα overexpressing HEK293 cells to verify th…

0301 basic medicineendocrine systemBisphenolDown-RegulationGene ExpressionEstrogen receptorBreast NeoplasmsEndocrine DisruptorsToxicologyCell Line03 medical and health sciences0302 clinical medicinePhenolsPlasticizersBCAS3Cell Line TumorHumansBenzhydryl CompoundsCell ProliferationInsulin-like growth factor 1 receptorPharmacologyEstradiolChemistryCell growthEstrogen Receptor alphaEstrogensCell cycleUp-RegulationHEK293 Cells030104 developmental biologyPRKCDMCF-7030220 oncology & carcinogenesisMCF-7 CellsCancer researchFemalehormones hormone substitutes and hormone antagonistsSignal TransductionToxicology and Applied Pharmacology
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Resveratrol and Vascular Function

2019

Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling. At the same time, resveratrol inhibits the synthesis of endothelin-1 and reduces oxidative stress in both endothelial cells and smooth muscle cells. Pathological stimuli-induced smooth muscle cell proliferation, vascular remodeling, and arterial stiffness can be ameliorated by resveratrol as well. In addition, resveratrol also modulates immune cell function, inhibition of immune cell infiltration into the vascular wall, and improves the function of perivascular adipose tissue. All…

0301 basic medicineendotheliumEndotheliumAdipose tissueBlood PressureReviewresveratrol030204 cardiovascular system & hematologyResveratrolsirtuin 1AntioxidantsMuscle Smooth VascularCatalysisvascular functionNitric oxidelcsh:ChemistryInorganic Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicinecardiovascular diseaseEnosmedicineAnimalsHumansPhysical and Theoretical ChemistryReceptorlcsh:QH301-705.5Molecular BiologyAntihypertensive AgentsSpectroscopybiologySirtuin 1Cell growthChemistryOrganic Chemistryfood and beveragesGeneral Medicinebiology.organism_classificationComputer Science ApplicationsCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999biology.proteinEndothelium Vascularendothelial nitic oxide synthaseInternational Journal of Molecular Sciences
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Protective Effect of Pogostone on 2,4,6-Trinitrobenzenesulfonic Acid-Induced Experimental Colitis via Inhibition of T Helper Cell

2017

Inflammatory bowel disease (IBD) is a chronic immune-related disease mainly caused by the disequilibrium of T helper (Th) cell paradigm? Pogostone (PO) is one of the major chemical constituents of Pogostemon cablin (Blanco) Benth. The present study aims to investigate the potential benefit of PO against IBD in a 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis model. PO treatment by enema significantly brought down the disease activity index (DAI) of the TNBS-challenged rats, which was manifested by the ameliorated inflammatory features including ulceration, adhesion, and edema. Hematoxylin-eosin (HE) staining and immunohistochemistry analysis showed that PO effectivel…

0301 basic medicineexperimental colitisCellPharmacologyInflammatory bowel diseaseProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound246-Trinitrobenzenesulfonic acidEdemamedicinePharmacology (medical)T helper cellOriginal ResearchPharmacologybiologyCell growthbusiness.industrylcsh:RM1-950pogostoneT helper cellmedicine.diseaseTNBSanti-inflammationdigestive system diseaseslcsh:Therapeutics. Pharmacology030104 developmental biologymedicine.anatomical_structurechemistryMyeloperoxidaseImmunologybiology.proteinmedicine.symptombusinessFrontiers in Pharmacology
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