Search results for "growth"

showing 10 items of 5134 documents

9-ING-41, a small-molecule glycogen synthase kinase-3 inhibitor, is active in neuroblastoma.

2018

Advanced stage neuroblastoma is a very aggressive pediatric cancer with limited treatment options and a high mortality rate. Glycogen Synthase Kinase-3β (GSK-3β) is a potential therapeutic target in neuroblastoma. Using immunohistochemical staining, we observed positive GSK-3β expression in 67% of human neuroblastomas (34 out of 51 cases). Chemically distinct GSK-3 inhibitors (AR-A014418, TDZD8 and 9-ING-41), suppressed the growth of neuroblastoma cells whereas 9-ING-41, a clinically relevant small molecule GSK-3β inhibitor with broad spectrum pre-clinical antitumor activity, being the most potent. Inhibition of GSK-3 resulted in a decreased expression of the antiapoptotic molecule XIAP and…

0301 basic medicineCancer ResearchIndolesMice NudeCell Growth ProcessesIrinotecanArticleMaleimides03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineGSK-3NeuroblastomaCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Enzyme InhibitorsGlycogen synthasePharmacologyGlycogen Synthase Kinase 3 betabiologyChemistryDrug Synergismmedicine.diseasePediatric cancerXenograft Model Antitumor AssaysXIAP030104 developmental biologyOncologyCell cultureApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinImmunohistochemistryFemaleAnti-cancer drugs
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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Dual Constant Domain-Fab: A novel strategy to improve half-life and potency of a Met therapeutic antibody

2016

The kinase receptor encoded by the Met oncogene is a sensible target for cancer therapy. The chimeric monovalent Fab fragment of the DN30 monoclonal antibody (MvDN30) has an odd mechanism of action, based on cell surface removal of Met via activation of specific plasma membrane proteases. However, the short half-life of the Fab, due to its low molecular weight, is a severe limitation for the deployment in therapy. This issue was addressed by increasing the Fab molecular weight above the glomerular filtration threshold through the duplication of the constant domains, in tandem (DCD-1) or reciprocally swapped (DCD-2). The two newly engineered molecules showed biochemical properties comparable…

0301 basic medicineCancer ResearchMice SCIDCancer targeted therapy0302 clinical medicineMice Inbred NODEpidermal growth factor receptorPhosphorylationbiologyChemistryImmunoglobulin Fab FragmentsAntibodies MonoclonalGeneral MedicineArticlesProto-Oncogene Proteins c-metHalf-lifeCell biologyOncology030220 oncology & carcinogenesisColonic NeoplasmsMetMolecular MedicineFemalemedicine.symptomSignal transductionAntibodySignal Transductionmedicine.drug_classColonAntibody; Cancer targeted therapy; Fab; Half-life; Met; Protein engineering; Cancer Research; Genetics; Molecular MedicineAntineoplastic AgentsMonoclonal antibody03 medical and health sciencesImmunoglobulin Fab FragmentsProtein DomainsCell Line TumormedicineGeneticsAnimalsHumansFabAntibodyCell growthMolecular biology030104 developmental biologyHEK293 CellsMechanism of actionHepatocyte Growth Factor ReceptorA549 Cellsbiology.proteinProtein engineering
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Imiquimod inhibits growth and induces differentiation of myeloid leukemia cell lines

2018

Background: The antitumoral effects of different Toll-like receptor (TLRs) agonists is mediated by activating immune responses to suppress tumors growth, although TLR ligands may also have a direct effect on tumoral cells. Given that TLR signaling induces hematopoietic cell differentiations this may serve as a novel differentiation therapeutic approach for AML. Methods: We investigated the effects of agonists for the ten human TLRs on the proliferation, apoptosis, cell cycle and differentiation of ten different types of myeloid leukemia cell lines (HL-60, U-937, KG-1, KG-1a, K-562, Kasumi-1, EOL-1, NB4, MOLM-13 and HEL). Proliferation was measured using the CellTiter 96 (R) Aqueous One Solu…

0301 basic medicineCancer ResearchMyeloidImiquimodlcsh:RC254-282Flow cytometry03 medical and health sciences0302 clinical medicineToll-like receptorGeneticsmedicineCytotoxic T cellMyeloid leukemia cell lineslcsh:QH573-671Toll-like receptorImiquimodmedicine.diagnostic_testChemistryCell growthlcsh:CytologyMyeloid leukemiaCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchPrimary Researchmedicine.drugCancer Cell International
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Isolation, culture and analysis of adult subependymal neural stem cells

2016

Individual cells dissected from the subependymal neurogenic niche of the adult mouse brain proliferate in medium containing basic fibroblast growth factor (bFGF) and/or epidermal growth factor (EGF) as mitogens, to produce multipotent clonal aggregates called neurospheres. These cultures constitute a powerful tool for the study of neural stem cells (NSCs) provided that they allow the analysis of their features and potential capacity in a controlled environment that can be modulated and monitored more accurately than in vivo. Clonogenic and population analyses under mitogen addition or withdrawal allow the quantification of the self-renewing and multilineage potency of these cells and the id…

0301 basic medicineCancer ResearchNeurogenesisCellular differentiationBasic fibroblast growth factorPopulationCell Culture TechniquesBiologyMice03 medical and health scienceschemistry.chemical_compoundNeural Stem CellsEpendymaNeurosphereSubependymal zoneAnimalsHumanseducationMolecular BiologyNeuronseducation.field_of_studyNeurogenesisCell DifferentiationCell BiologyNeural stem cellCell biologyAdult Stem Cells030104 developmental biologychemistryImmunologyDevelopmental BiologyAdult stem cellDifferentiation
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Multiple myeloma-derived exosomes are enriched of amphiregulin (AREG) and activate the epidermal growth factor pathway in the bone microenvironment l…

2019

Background Multiple myeloma (MM) is a clonal plasma cell malignancy associated with osteolytic bone disease. Recently, the role of MM-derived exosomes in the osteoclastogenesis has been demonstrated although the underlying mechanism is still unknown. Since exosomes-derived epidermal growth factor receptor ligands (EGFR) are involved in tumor-associated osteolysis, we hypothesize that the EGFR ligand amphiregulin (AREG) can be delivered by MM-derived exosomes and participate in MM-induced osteoclastogenesis. Methods Exosomes were isolated from the conditioned medium of MM1.S cell line and from bone marrow (BM) plasma samples of MM patients. The murine cell line RAW264.7 and primary human CD1…

0301 basic medicineCancer ResearchOsteoclastsPlasma cellInterleukin 8ExosomesLigandsMice0302 clinical medicineEpidermal growth factorOsteogenesisMultiple myelomaBone diseaseTumor MicroenvironmentEpidermal growth factor receptorbiologyChemistryAntibodies MonoclonalOsteoblastCell DifferentiationHematologylcsh:Diseases of the blood and blood-forming organslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensErbB Receptorsmedicine.anatomical_structureOncology030220 oncology & carcinogenesislcsh:RC254-282Amphiregulin03 medical and health sciencesAmphiregulinOsteoclastCell Line TumormedicineCell AdhesionAnimalsHumansMolecular BiologyOsteoblastsEpidermal Growth Factorlcsh:RC633-647.5Epidermal growth factor receptorResearchMesenchymal stem cellInterleukin-8Mesenchymal Stem CellsMicrovesiclesExosome030104 developmental biologyRAW 264.7 CellsCancer researchbiology.protein
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2021

The prognosis for advanced prostate carcinoma (PCa) remains poor due to development of therapy resistance, and new treatment options are needed. Shikonin (SHI) from Traditional Chinese Medicine has induced antitumor effects in diverse tumor entities, but data related to PCa are scarce. Therefore, the parental (=sensitive) and docetaxel (DX)-resistant PCa cell lines, PC3, DU145, LNCaP, and 22Rv1 were exposed to SHI [0.1–1.5 μM], and tumor cell growth, proliferation, cell cycling, cell death (apoptosis, necrosis, and necroptosis), and metabolic activity were evaluated. Correspondingly, the expression of regulating proteins was assessed. Exposure to SHI time- and dose-dependently inhibited tum…

0301 basic medicineCancer ResearchProgrammed cell deathCell cycle checkpointChemistryNecroptosisfungiCellCell cycleurologic and male genital diseases03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinemedicine.anatomical_structureOncologyDU145030220 oncology & carcinogenesisLNCaPCancer researchmedicineGrowth inhibitionCancers
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Molecular Engineering Strategies Tailoring the Apoptotic Response to a MET Therapeutic Antibody

2020

The MET oncogene encodes a tyrosine kinase receptor involved in the control of a complex network of biological responses that include protection from apoptosis and stimulation of cell growth during embryogenesis, tissue regeneration, and cancer progression. We previously developed an antagonist antibody (DN30) inducing the physical removal of the receptor from the cell surface and resulting in suppression of the biological responses to MET. In its bivalent form, the antibody displayed a residual agonist activity, due to dimerization of the lingering receptors, and partial activation of the downstream signaling cascade. The balance between the two opposing activities is variable in different…

0301 basic medicineCancer ResearchProgrammed cell deathlcsh:RC254-282ArticleReceptor tyrosine kinase03 medical and health sciences0302 clinical medicineMET oncogenemedicineantibodiesAntibodies; Apoptosis; MET oncogene; MET targeted therapyReceptorbiologyCell growthChemistryapoptosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmet targeted therapyCell biology030104 developmental biologyOncology<i>met</i> oncogeneApoptosis030220 oncology & carcinogenesisCancer cellbiology.proteinHepatocyte growth factorAntibodymedicine.drugCancers
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Tumor-Associated Fibroblasts Promote HER2-Targeted Therapy Resistance through FGFR2 Activation

2020

AbstractPurpose:Despite the therapeutic success of existing HER2-targeted therapies, tumors invariably relapse. This study aimed at identifying new mechanisms responsible for HER2-targeted therapy resistance.Experimental Design:We have used a platform of HER2-targeted therapy–resistant cell lines and primary cultures of healthy and tumor-associated fibroblasts (TAF) to identify new potential targets related to tumor escape from anti-HER2 therapies.Results:We have shown that TAFs promote resistance to HER2-targeted therapies. TAFs produce and secrete high levels of FGF5, which induces FGFR2 activation in the surrounding breast cancer cells. FGFR2 transactivates HER2 via c-Src, leading to res…

0301 basic medicineCancer ResearchReceptor ErbB-2medicine.medical_treatmentMice NudeBreast NeoplasmsDrug resistanceTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerCancer-Associated FibroblastsTrastuzumabCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineNeoplasmAnimalsHumansReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesneoplasmsbusiness.industryLapatinibTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysSurvival Rate030104 developmental biologyOncologyTumor EscapeApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemaleSignal transductionNeoplasm Recurrence Localbusinessmedicine.drugSignal Transduction
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