Search results for "CANCER STEM CELL"

showing 10 items of 220 documents

IL-4 protects tumor cells from anti-CD95 and chemotherapeutic agents via up-regulation of antiapoptotic proteins

2004

Abstract We recently proposed that Th1 and Th2 cytokines exert opposite effects on the pathogenesis and clinical outcome of organ-specific autoimmunity by altering the expression of genes involved in target cell survival. Because a Th2 response against tumors is associated with poor prognosis, we investigated the ability of IL-4 to protect tumor cells from death receptor- and chemotherapy-induced apoptosis. We found that IL-4 treatment significantly reduced CD95 (Fas/APO-1)- and chemotherapeutic drug-induced apoptosis in prostate, breast, and bladder tumor cell lines. Analysis of antiapoptotic protein expression revealed that IL-4 stimulation resulted in up-regulation of cellular (c) FLIP/F…

MaleINFILTRATING LYMPHOCYTESCell SurvivalImmunologyCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinAntineoplastic AgentsApoptosisBreast NeoplasmsCARCINOMA-CELLSBiologySIGNALING PATHWAYSDownregulation and upregulationCell Line TumorImmunology and AllergyHumansfas ReceptorNON-HODGKINS-LYMPHOMACANCER PATIENTSReceptorBCL-2 PROTEINInterleukin 4EtoposideIL-4 apoptosis cancer stem cellsSettore MED/04 - Patologia GeneraleCHRONIC LYMPHOCYTIC-LEUKEMIAIntracellular Signaling Peptides and ProteinsAntibodies MonoclonalProstatic NeoplasmsFas receptorRecombinant ProteinsCell biologyUp-RegulationProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureFlipCancer researchT-CELLSCamptothecinFemaleInterleukin-4FLICE-INHIBITORY PROTEINSignal transductionCarrier ProteinsRENAL-CELL
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Modeling human osteosarcoma in mice through 3AB‐OS cancer stem cell xenografts

2012

Osteosarcoma is the second leading cause of cancer-related death for children and young adults. In this study, we have subcutaneously injected—with and without matrigel—athymic mice (Fox1nu/nu) with human osteosarcoma 3AB-OS pluripotent cancer stem cells (CSCs), which we previously isolated from human osteosarcoma MG63 cells. Engrafted 3AB-OS cells were highly tumorigenic and matrigel greatly accelerated both tumor engraftment and growth rate. 3AB-OS CSC xenografts lacked crucial regulators of beta-catenin levels (E-cadherin, APC, and GSK-3beta), and crucial factors to restrain proliferation, resulting therefore in a strong proliferation potential. During the first weeks of engraftment 3AB-…

MaleIntegrin beta ChainsXENOGRAFTNudeAnimals; Bone Neoplasms; Collagen; Drug Combinations; Focal Adhesion Kinase 1; Gene Expression Regulation Neoplastic; Humans; Injections Subcutaneous; Integrin beta Chains; Laminin; Male; Mice; Mice Nude; Neoplasm Transplantation; Neoplastic Stem Cells; Osteosarcoma; Pluripotent Stem Cells; Proteoglycans; Proto-Oncogene Proteins c-akt; Signal Transduction; Transplantation Heterologous; Tumor Markers Biological3AB-OS CSCSBiochemistryMiceInduced pluripotent stem cellTumor MarkersOsteosarcomaHeterologousSubcutaneousXIAPGene Expression Regulation NeoplasticDrug CombinationsANIMAL MODELSNeoplastic Stem CellsOsteosarcomaProteoglycansCollagenMATRIGELSignal TransductionPluripotent Stem CellsInjections SubcutaneousTransplantation HeterologousMice NudeBone NeoplasmsBiologyInjectionsCyclin D2Cancer stem cellBiomarkers TumormedicineAnimalsHumansMolecular BiologyProtein kinase BNeoplasticTransplantationMatrigelMesenchymal stem cellCell BiologyBiologicalmedicine.disease3AB-OS CSCS; OSTEOSARCOMA; XENOGRAFT; MATRIGEL; ANIMAL MODELSGene Expression RegulationFocal Adhesion Kinase 1ImmunologyCancer researchLamininProto-Oncogene Proteins c-aktNeoplasm TransplantationJournal of Cellular Biochemistry
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Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mtor pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

2011

Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described …

MaleMAPK/ERK pathwayAgingMAP Kinase Signaling SystemCancer aging RAF MEK mTORApoptosisReviewBiologyPI3KModels BiologicalApoptosis; Cancer; Kinases; MEK; MTOR; PI3K; Protein phosphorylation; RAF; Signal transductionMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCancer stem cellNeoplasmscancerAnimalsHumansPTENProtein kinase BCellular SenescencePI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesKinaseTOR Serine-Threonine KinasesapoptosisPTEN PhosphohydrolaseRafCell BiologyMEKprotein phosphorylation3. Good healthCell biologyCrosstalk (biology)kinases030220 oncology & carcinogenesisMutationmTORCancer researchbiology.proteinFemaleraf KinasesProto-Oncogene Proteins c-aktCell agingsignal transduction
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Aurora-A Is Essential for the Tumorigenic Capacity and Chemoresistance of Colorectal Cancer Stem Cells

2010

Abstract Colorectal cancer stem cells (CR-CSC) are responsible for the generation and maintenance of intestinal tumors and are highly resistant to conventional chemotherapeutic agents. Aurora-A, a serine-threonine kinase involved in mitosis regulation, plays multiple key functions in tumor initiation and progression. We found that Aurora-A is overexpressed in primary colorectal tumor cells, in the CR-CSC fraction, and in stem cell–derived differentiated cells, compared with normal colon tissue. Aurora-A expression was functionally linked to centrosome amplification in CR-CSC, as indicated by the decrease in cells with multiple centrosomes that followed Aurora-A silencing. Knockdown of Auror…

MaleOncologyCancer Researchmedicine.medical_specialtyColorectal cancerCellular differentiationcolorectal cancer stem cellsMice NudeCell Growth ProcessesTumor initiationProtein Serine-Threonine KinasesBiologyMiceAurora KinasesCell MovementCancer stem cellInternal medicinemedicineAnimalsHumansCytotoxic T cellGene silencingMitosisAgedAurora Kinase ACentrosomeCell CycleGene AmplificationMiddle Agedmedicine.diseaseOncologyDrug Resistance NeoplasmGene Knockdown TechniquesNeoplastic Stem CellsCancer researchFemalebiological phenomena cell phenomena and immunityStem cellColorectal NeoplasmsCancer Research
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Roles of signaling pathways in drug resistance, cancer initiating cells and cancer progression and metastasis

2014

The EGFR/PI3K/PTEN/Akt/mTORC pathway plays prominent roles in malignant transformation, prevention of apoptosis, drug resistance, cancer initiating cells (CICs) and metastasis. The expression of this pathway is frequently altered in breast and other cancers due to mutations at or aberrant expression of: HER2, EGFR1, PIK3CA, and PTEN as well as other oncogenes and tumor suppressor genes. miRs and epigenetic mechanisms of gene regulation are also important events which regulate this pathway. In some breast cancer cases, mutations at certain components of this pathway (e.g., PIK3CA) are associated with a better prognosis than breast cancers lacking these mutations. The expression of this pathw…

MaleOncologyCancer Researchmedicine.medical_treatmentTargeted therapyMetastasisTargeted therapyBreast cancerNeoplasmsNeoplasm MetastasisCancer stem cellsMedicine (all)Neoplasm ProteinsNeoplasm MetastasiGene Expression Regulation NeoplasticCell Transformation NeoplasticMolecular MedicineFemaleHormonal therapyHumanSignal Transductionmedicine.medical_specialtyEGFRBiologyNeoplasm ProteinBreast cancerGeneticCancer stem cellInternal medicineHER2GeneticsmedicineAnimalsHumansPTENMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationAnimalCancer stem cellTherapy resistanceCancermedicine.diseaseERDrug Resistance NeoplasmBreast cancer; Cancer stem cells; EGFR; ER; HER2; Hormonal therapy; Targeted therapy; Therapy resistancebiology.proteinCancer researchNeoplasm
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Bone morphogenetic protein 4 induces differentiation of colorectal cancer stem cells and increases their response to chemotherapy in mice.

2010

BACKGROUND & AIMS: The limited clinical response observed in many patients with colorectal cancer may be related to the presence of chemoresistant colorectal can- cer stem cells (CRC-SCs). Bone morphogenetic protein 4 (BMP4) promotes the differentiation of normal colonic stem cells. We investigated whether BMP4 might be used to induce differentiation of CRC-SCs and for therapeutic purposes. METHODS: CRC-SCs were isolated from 25 tumor samples based on expression of CD133 or using a selection culture medium. BMP4 expression and activity on CRC-SCs were evaluated in vitro; progeny of the stem cells were evaluated by immunofluorescence, immuno- blot, and flow cytometry analyses. The potential …

MaleOrganoplatinum CompoundsCellular differentiationDrug ResistanceApoptosisBone Morphogenetic Protein 4Colon Cancer; Drug Resistance; Neoplasia; Tumor Resistance to Chemotherapy; AC133 Antigen; Adenomatous Polyposis Coli; Aged; Aged 80 and over; Animals; Antigens CD; Antineoplastic Agents; Apoptosis; Bone Morphogenetic Protein 4; Cell Differentiation; Cells Cultured; Colorectal Neoplasms; Female; Fluorouracil; Glycoproteins; Humans; Male; Mice; Microsatellite Instability; Middle Aged; Mutation; Neoplastic Stem Cells; Organoplatinum Compounds; PTEN Phosphohydrolase; Peptides; Phosphatidylinositol 3-Kinase; Proto-Oncogene Proteins c-akt; Smad4 Protein; GastroenterologyMice80 and overBone morphogenetic protein receptorAC133 AntigenCells CulturedSmad4 ProteinAged 80 and overCulturedColon Cancerintegumentary systemGastroenterologyCell DifferentiationBMP4 colon stem cellsMiddle AgedCDOxaliplatinTumor Resistance to ChemotherapyBone morphogenetic protein 4Adenomatous Polyposis Coliembryonic structuresNeoplastic Stem CellsFemaleMicrosatellite InstabilityFluorouracilStem cellColorectal Neoplasmsanimal structuresCellsAntineoplastic AgentsBiologyBone morphogenetic proteinSettore MED/04 - PATOLOGIA GENERALECancer stem cellAntigens CDPTENAnimalsHumansAntigensneoplasmsPI3K/AKT/mTOR pathwayAgedGlycoproteinsNeoplasiaHepatologyPTEN Phosphohydrolasedigestive system diseasesMutationCancer researchbiology.proteinPhosphatidylinositol 3-KinasePeptidesProto-Oncogene Proteins c-aktGastroenterology
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A novel CXCR4 antagonist counteracts paradoxical generation of cisplatin-induced pro-metastatic niches in lung cancer.

2021

Platinum-based chemotherapy remains widely used in advanced non-small cell lung cancer (NSCLC) despite experimental evidence of its potential to induce long-term detrimental effects, including the promotion of pro-metastatic microenvironments. In this study, we investigated the interconnected pathways underlying the promotion of cisplatin-induced metastases. In tumor-free mice, cisplatin treatment resulted in an expansion in the bone marrow of CCR2+CXCR4+Ly6Chigh inflammatory monocytes (IMs) and an increase in lung levels of stromal SDF-1, the CXCR4 ligand. In experimental lung metastasis assays, cisplatin-induced IMs promoted the extravasation of tumor cells and the expansion of CD133+CXCR…

MaleReceptors CXCR4Stromal cellLung NeoplasmsSettore MED/08 - Anatomia PatologicaMonocytesMetastasisMiceCarcinoma Non-Small-Cell LungCell Line TumorDrug DiscoveryGeneticsMedicineSettore MED/05 - Patologia ClinicaAnimalsHumansDrug InteractionsAC133 AntigenNeoplasm MetastasisLung cancerMolecular BiologyPharmacologyCisplatinCXCR4 antagonistchemotherapy combination therapy inflammatory monocytes lung cancer stem cells metastasis peptide anti-CXCR4 SDF-1/CXCR4 axisbusiness.industrymedicine.diseasePrimary tumorXenograft Model Antitumor AssaysExtravasationChemokine CXCL12medicine.anatomical_structureRAW 264.7 CellsA549 CellsCancer researchNeoplastic Stem CellsMolecular MedicineBone marrowCisplatinbusinessPeptidesmedicine.drugMolecular therapy : the journal of the American Society of Gene Therapy
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Identification and phenotypic characterization of a subpopulation of T84 human colon cancer cells, after selection on activated endothelial cells

2004

The extravasation of metastatic cells is regulated by molecular events involving the initial adhesion of tumor cells to the endothelium and subsequently the migration of the cells in the host connective tissue. The differences in metastatic ability could be attributed to properties intrinsic of the various primary tumor types. Thus, the clonal selection of neoplastic cells during cancer progression results in cells better equipped for survival and formation of colonies in secondary sites. A cell line (T84SF) exhibiting an altered phenotypic appearance was selected from a colon cancer cell line (T84) by repetitive plating on TNFα-activated human endothelial cells and subsequent selection for…

MaleUmbilical VeinsPhysiologyCellular differentiationClinical BiochemistryMice NudeApoptosisCell CommunicationMicechemistry.chemical_compoundCancer stem cellCell Line TumorCell AdhesionAnimalsHumansNeoplasm InvasivenessEnzyme InhibitorsNeoplasm MetastasisPhosphorylationCD40biologyCell growthTyrosine phosphorylationCell BiologyCell biologyEndothelial stem cellPhenotypesrc-Family KinaseschemistryCell cultureColonic NeoplasmsMetalloproteasesbiology.proteinTyrosineEndothelium VascularCell DivisionNeoplasm TransplantationProto-oncogene tyrosine-protein kinase SrcJournal of Cellular Physiology
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Cancer Clonal Evolution and Intra-tumor Heterogeneity

2017

Despite recent advances in understanding cancer onset mechanisms and development of new therapeutic approaches, however, the resistance of tumor cells to different therapies represents the main obstacle to the successful treatment, resulting in poor prognosis and tumor recurrence. Currently, understanding the causes underlying this resistance is the main objective of oncology research in recent years. Tumors are not uniform diseases but heterogeneous entities consisting of cell populations called clones, with different genetic and molecular characteristics. Indeed, most of cancers shows usually a single clonal origin at the early stages of the disease, but, in advanced stages, tumors may in…

Mechanism (biology)Cancer stem cellMelanomamedicineCancer researchCancerGenetic variabilityDiseaseDrug resistanceBiologymedicine.diseaseSomatic evolution in cancer
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MicroRNA-29b-1 is involved in self-renewal and fate decisions of human osteosarcoma 3AB-OS cancer stem cells

2014

Emerging evidence suggests that treatments targeting cancer stem cells (CSCs) within a tumor can halt cancer and improve patient survival. Moreover, identification of CSC-related MicroRNAs (miRNAs) would provide information for a better understanding of CSCs. miR-29 family is a class of miRNAs aberrantly expressed in multiple cancers. They are frequently down-regulated in osteosarcoma (OS), the most common form of childhood cancer with a potent metastasizing potential. 3AB-OS CSC, a human pluripotent CSC line by us produced from the human osteosarcoma MG63 cells (1) is a useful model to study CSC origin and roles (2). Previously, we have shown that in 3AB-OS CSCs miR-29b is potently down-re…

MicroRNA-29b-1 self-renewal human osteosarcoma 3AB-OS cancer stem cells
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