Search results for " breast"

showing 10 items of 610 documents

Is Danggui Safe to be Taken by Breast Cancer Patients?-A Skepticism Finally Answered by Comprehensive Preclinical Evidence.

2019

Angelica sinensis (AS, Danggui) has long been regarded to stimulate breast cancer growth; hence, the use of AS in breast cancer patients remains a major concern for both patients and practitioners. Since safety studies of herbs would be unethical to carry out in patients, the present study aimed to investigate the potential unsafe effects of AS in a systematic pre-clinical approach. Human breast cancer cells, breast orthotopic tumor-bearing mouse models, as well as primary breast cancer cells from patients’ tumors were used to evaluate the effect of AS hot water extract on the progression of breast tumors and/or growth of breast cancer cells. We showed that AS is not that stimulatory in bre…

0301 basic medicineOncologysafetymedicine.medical_specialtyprimary breast cancer cellsmedicine.drug_classXenotransplantationmedicine.medical_treatmentTraditional Chinese medicine03 medical and health sciences0302 clinical medicineBreast cancerbreast cancerInternal medicinemedicinePharmacology (medical)skin and connective tissue diseasesOriginal ResearchPharmacologySafety studiesbusiness.industrylcsh:RM1-950Angelica sinensisChinese herbal medicinesmedicine.diseaselcsh:Therapeutics. Pharmacology030104 developmental biologyEstrogen030220 oncology & carcinogenesisCancer cellestrogenic herbsBreast cancer cellsPrimary breast cancerbusinessFrontiers in pharmacology
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miR-9 and miR-200 regulate PDGFRβ-mediated endothelial differentiation of tumor cells in triple-negative breast cancer

2016

Abstract Organization of cancer cells into endothelial-like cell-lined structures to support neovascularization and to fuel solid tumors is a hallmark of progression and poor outcome. In triple-negative breast cancer (TNBC), PDGFRβ has been identified as a key player of this process and is considered a promising target for breast cancer therapy. Thus, we aimed at investigating the role of miRNAs as a therapeutic approach to inhibit PDGFRβ-mediated vasculogenic properties of TNBC, focusing on miR-9 and miR-200. In MDA-MB-231 and MDA-MB-157 TNBC cell lines, miR-9 and miR-200 promoted and inhibited, respectively, the formation of vascular-like structures in vitro. Induction of endogenous miR-9…

0301 basic medicinePathologymedicine.medical_specialtyCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueTriple Negative Breast NeoplasmsMice SCIDBiologySettore MED/08 - Anatomia PatologicaPolymerase Chain ReactionNeovascularizationReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesMice0302 clinical medicinemicroRNAmedicineAnimalsHumansTriple-negative breast cancerIn Situ HybridizationRegulation of gene expressionNeovascularization PathologicCancerEndothelial CellsCell Differentiationmedicine.diseaseImmunohistochemistryGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyOncologyOncology; Cancer Research030220 oncology & carcinogenesisGene Knockdown TechniquesCancer cellCancer researchHeterograftsEctopic expressionFemalemedicine.symptom
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MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation

2017

Summary Most patients with advanced triple-negative breast cancer (TNBC) develop drug resistance. MYC and MCL1 are frequently co-amplified in drug-resistant TNBC after neoadjuvant chemotherapy. Herein, we demonstrate that MYC and MCL1 cooperate in the maintenance of chemotherapy-resistant cancer stem cells (CSCs) in TNBC. MYC and MCL1 increased mitochondrial oxidative phosphorylation (mtOXPHOS) and the generation of reactive oxygen species (ROS), processes involved in maintenance of CSCs. A mutant of MCL1 that cannot localize in mitochondria reduced mtOXPHOS, ROS levels, and drug-resistant CSCs without affecting the anti-apoptotic function of MCL1. Increased levels of ROS, a by-product of a…

0301 basic medicinePhysiologyMice NudeTriple Negative Breast NeoplasmsOxidative phosphorylationTumor initiationMitochondrionBiologyOxidative PhosphorylationArticleProto-Oncogene Proteins c-myc03 medical and health sciencesCancer stem cellCell Line TumorAnimalsHumansMCL1Molecular BiologyTriple-negative breast cancerchemistry.chemical_classificationReactive oxygen speciesCell BiologyMitochondria030104 developmental biologychemistryDrug Resistance NeoplasmNeoplastic Stem CellsCancer researchMyeloid Cell Leukemia Sequence 1 ProteinFemaleStem cellReactive Oxygen SpeciesCell Metabolism
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Anticancer activity of biogenerated silver nanoparticles: an integrated proteomic investigation

2018

Silver nanoparticles (AgNPs), embedded into a specific polysaccharide (EPS), were biogenerated by Klebsiella oxytoca DSM 29614 under aerobic (AgNPs-EPSaer) and anaerobic conditions (AgNPs-EPSanaer). Both AgNPs-EPS matrices were tested by MTT assay for cytotoxic activity against human breast (SKBR3 and 8701-BC) and colon (HT-29, HCT 116 and Caco-2) cancer cell lines, revealing AgNPs-EPSaer as the most active, in terms of IC50, with a more pronounced efficacy against breast cancer cell lines. Therefore, colony forming capability, morphological changes, generation of reactive oxygen species (ROS), induction of apoptosis and autophagy, inhibition of migratory and invasive capabilities and prote…

0301 basic medicineProgrammed cell deathSettore BIO/11 - Biologia MolecolareMitochondrionmedicine.disease_causeSettore BIO/19 - Microbiologia Generale03 medical and health sciencesproteomicsbreast cancer cellmedicineMTT assaySettore BIO/06 - Anatomia Comparata E Citologiabacteriachemistry.chemical_classificationAnticancer activity; Bacteria; Breast cancer cells; Proteomics; Silver nanoparticles (AgNPs); OncologyReactive oxygen speciesBreast cancer cellsChemistryAutophagysilver nanoparticles (AgNPs)Cell biology030104 developmental biologyanticancer activitysilver nanoparticles (AgNPs); bacteria; breast cancer cells; anticancer activity; proteomicsOncologyApoptosisSKBR3Oxidative stressResearch Paper
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Cytotoxic activity of the histone deacetylase 3-Selective inhibitor Pojamide on MDA-MB-231 triple-negative breast cancer cells

2019

We examined the effects of the ferrocene-based histone deacetylase-3 inhibitor Pojamide (N1-(2-aminophenyl)-N8-ferrocenyloctanediamide) and its two derivatives N1-(2-aminophenyl)-N6-ferrocenyladipamide and N1-(2-aminophenyl)-N8-ferroceniumoctanediamide tetrafluoroborate on triple-negative MDA-MB-231 breast cancer cells. Viability/growth assays indicated that only the first two compounds at 70 &mu

0301 basic medicineQD0901Triple Negative Breast Neoplasmslcsh:Chemistry0302 clinical medicinebreast cancer cellmitochondrial transmembrane potentialCytotoxic T cellQDSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopyTriple-negative breast cancerreactive oxygen speciesCell DeathChemistryHistone deacetylase inhibitorQapoptosisGeneral MedicineCell cycle3. Good healthComputer Science Applications030220 oncology & carcinogenesisFemalecell cycleProgrammed cell deathautophagymedicine.drug_classCell SurvivalCatalysisArticleHistone DeacetylasesInorganic Chemistry03 medical and health sciencesCell Line TumormedicineBiomarkers TumorHumansViability assayPhysical and Theoretical ChemistryMolecular Biologyhistone deacetylase inhibitorcell viabilityOrganic ChemistryAutophagyapoptosiMatrix MetalloproteinasesHistone Deacetylase InhibitorsSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999ApoptosisCancer researchQD0146breast cancer cells
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Biological Effect of a Hybrid Anticancer Agent Based on Kinase and Histone Deacetylase Inhibitors on Triple-Negative (MDA-MB231) Breast Cancer Cells

2016

We examined the effects of the histone deacetylase inhibitor (HDACi) suberoylanilide\ud hydroxamic acid (SAHA) combined with the vascular endothelial growth factor receptor-1/2 inhibitor\ud (3Z)-5-hydroxy-3-(1H-pyrrol-2-ylmethylidene)-2,3-dihydro-1H-indol-2-one on MDA-MB-231 breast\ud cancer cells (triple-negative) in the form of both a cocktail of the separate compounds and a chemically\ud synthesized hybrid (N-hydroxy-N'-[(3Z)-2-oxo-3-(1H-pyrrol-2-ylmethylidene)-2,3-dihydro-1H-indol-\ud 5-yl]octanediamide). Comparative flow cytometric and Western blot analyses were performed on\ud cocktail- and hybrid-treated cells to evaluate cell cycle distribution, autophagy/apoptosis modulation,\ud an…

0301 basic medicineVascular Endothelial Growth Factor AIndolesCytotoxicityTriple Negative Breast Neoplasmsbreast cancer; MDA-MB231 cells; histone deacetylase inhibitor; vascular endothelial growth factor receptor-2 inhibitor; cytotoxicity; cell cycle; apoptosis; autophagy; mitochondrial metabolismHydroxamic AcidsCatalysi0302 clinical medicineBreast cancerTumor Cells CulturedCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaSpectroscopyVorinostatVascular endothelial growth factor receptor-2 inhibitorApoptosis; Autophagy; Breast cancer; Cell cycle; Cytotoxicity; Histone deacetylase inhibitor; MDA-MB231 cells; Mitochondrial metabolism; Vascular endothelial growth factor receptor-2 inhibitor; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryKinaseHistone deacetylase inhibitorapoptosisComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineCell cycleFlow CytometryComputer Science ApplicationsCell biologyMDA-MB231 cell030220 oncology & carcinogenesisFemaleQD0241Programmed cell deathmedicine.drug_classCell SurvivalBlotting WesternAntineoplastic AgentsBiologyCell cycleCatalysisArticleInorganic Chemistry03 medical and health sciencesmedicineAutophagyHumansPhysical and Theoretical ChemistryProtein Kinase InhibitorsMolecular BiologyQD0415Histone deacetylase inhibitorAutophagyOrganic ChemistryApoptosiHistone Deacetylase Inhibitors030104 developmental biologyApoptosisMitochondrial metabolismMDA-MB231 cellsHistone deacetylaseInternational Journal of Molecular Sciences; Volume 17; Issue 8; Pages: 1235
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Antiproliferative and pro-apoptotic activity of melatonin analogues on melanoma and breast cancer cells

2017

// Giuliana Gatti 1, * , Valeria Lucini 2, * , Silvana Dugnani 2 , Angela Calastretti 1 , Gilberto Spadoni 3 , Annalida Bedini 3 , Silvia Rivara 4 , Marco Mor 4 , Gianfranco Canti 1 , Francesco Scaglione 2 and Annamaria Bevilacqua 1 1 Department of Medical Biotechnology and Translational Medicine, Universita degli Studi di Milano, Milan, Italy 2 Department of Oncology and Hemato-oncology, Universita degli Studi di Milano, Milan, Italy 3 Department of Biomolecular Sciences, Universita degli Studi di Urbino “Carlo Bo”, Urbino, Italy 4 Department of Food and Drug, Universita degli Studi di Parma, Parma, Italy * Authors contributed equally to this work Correspondence to: Annamaria Bevilacqua, e…

0301 basic medicineanti-cancer drugs; breast cancer; melanoma; melatonin analogues; melatonin receptorsPharmacologyMelatonin03 medical and health sciencesbreast cancer0302 clinical medicineBreast cancerIn vivomelatonin receptorsmelanomaMedicineCytotoxic T cellReceptoranti-cancer drugsbusiness.industryMelanomamelatonin analoguesmedicine.disease030104 developmental biologyOncologyApoptosis030220 oncology & carcinogenesisCancer cellbusinesshormones hormone substitutes and hormone antagonistsResearch Papermedicine.drugOncotarget
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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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MiR-24 induces chemotherapy resistance and hypoxic advantage in breast cancer

2017

// Giuseppina Roscigno 1, 2, * , Ilaria Puoti 1, 2, * , Immacolata Giordano 1 , Elvira Donnarumma 3 , Valentina Russo 1 , Alessandra Affinito 1 , Assunta Adamo 1 , Cristina Quintavalle 1, 2 , Matilde Todaro 4 , Maria dM Vivanco 5 , Gerolama Condorelli 1, 2 1 Department of Molecular Medicine and Medical Biotechnology, “Federico II” University of Naples, Naples, Italy 2 IEOS, CNR, Naples, Italy 3 IRCCS-SDN, Naples, Italy 4 Department of Pathobiology and Medical Biotechnology, University of Palermo, Palermo, Italy 5 CIC bioGUNE, Centre for Cooperative Research in Biosciences, Derio, Spain * These authors have contributed equally to the paper as first authors Correspondence to: Gerolama Condore…

0301 basic medicinecancer stem cellsApoptosisStem cell markermedicine.disease_causemicroRNAs Breast cancer Cancer stem cells BimL FIH1Mixed Function OxygenasesAntineoplastic Agent0302 clinical medicineCell MovementTumor Cells CulturedCell Self RenewalMixed Function OxygenaseBimLmicroRNACell HypoxiamicroRNAsGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisNeoplastic Stem CellsFemaleBreast NeoplasmAdult stem cellHumanResearch PaperFIH1BimL; FIH1; breast cancer; cancer stem cells; microRNAsAntineoplastic AgentsBreast Neoplasms03 medical and health sciencesBreast cancerbreast cancerDownregulation and upregulationCancer stem cellmicroRNAmedicineBiomarkers TumorHumansCell Proliferationbusiness.industryCancer stem cellApoptosiRepressor Proteinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitMolecular medicineRepressor Proteins030104 developmental biologyDrug Resistance NeoplasmImmunologyCancer researchNeoplastic Stem CellCisplatinCarcinogenesisbusiness
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Aberrantly Expressed Embryonic Protein NODAL Alters Breast Cancer Cell Susceptibility to γδ T Cell Cytotoxicity

2020

Gamma delta (γδ) T cells kill transformed cells, and increased circulating γδ T cells levels correlate with improved outcome in cancer patients; however, their function within the breast tumor microenvironment (TME) remains controversial. As tumors progress, they begin to express stem-cell associated proteins, concomitant with the emergence of therapy resistant metastatic disease. For example, invasive breast cancers often secrete the embryonic morphogen, NODAL. NODAL has been shown to promote angiogenesis, therapy resistance and metastasis in breast cancers. However, to date, little is known about how this secreted protein may interact with cells in the TME. Herein we explore how NODAL in …

0301 basic medicinelcsh:Immunologic diseases. AllergyNodal ProteinAngiogenesisT cellImmunologytumor evasionTriple Negative Breast NeoplasmsBiologyMetastasis03 medical and health sciences0302 clinical medicineTumor Microenvironmentmedicineinvasive ductal carcinomaHumansImmunology and Allergygamma delta T cellsIntraepithelial LymphocytesTriple-negative breast cancerOriginal ResearchAgedAged 80 and overT-cell receptorCancerReceptors Antigen T-Cell gamma-deltaMiddle Agedmedicine.diseasegammadelta030104 developmental biologymedicine.anatomical_structureCell culturetriple negative breast cancerMICACancer researchFemaleTumor EscapeNODALNODALlcsh:RC581-607030215 immunologyFrontiers in Immunology
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