Search results for "APOPTOSIS"

showing 10 items of 1809 documents

Transcriptional Profiles and Stromal Changes Reveal Bone Marrow Adaptation to Early Breast Cancer in Association with Deregulated Circulating microRN…

2020

Abstract The presence of a growing tumor establishes a chronic state of inflammation that acts locally and systemically. Bone marrow responds to stress signals by expanding myeloid cells endowed with immunosuppressive functions, further fostering tumor growth and dissemination. How early in transformation the cross-talk with the bone marrow begins and becomes detectable in blood is unknown. Here, gene expression profiling of the bone marrow along disease progression in a spontaneous model of mammary carcinogenesis demonstrates that transcriptional modifications in the hematopoietic compartment occurred as early as preinvasive disease stages. The transcriptional profile showed downregulation…

0301 basic medicineCancer ResearchMyeloidStromal cellInflammationApoptosisBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaCXCR403 medical and health sciencesMice0302 clinical medicineBone MarrowmedicineBiomarkers TumorTumor Cells CulturedAnimalsHumansCirculating MicroRNACell ProliferationMice Inbred BALB CInnate immune systemGene Expression ProfilingAcquired immune systemAdaptation PhysiologicalXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticHaematopoiesis030104 developmental biologymedicine.anatomical_structureOncologyTrascriptional profiles early brest cancer microRNAs030220 oncology & carcinogenesisCancer researchFemaleBone marrowmedicine.symptomStromal CellsTranscriptomeCancer research
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Nicotinamide Phosphoribosyltransferase Acts as a Metabolic Gate for Mobilization of Myeloid-Derived Suppressor Cells

2019

Abstract Cancer induces alteration of hematopoiesis to fuel disease progression. We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow. NAMPT inhibits CXCR4 through a NAD/Sirtuin 1–mediated inactivation of HIF1α-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide. Pharmacologic inhibition or myeloid-specific ablation …

0301 basic medicineCancer ResearchMyeloidmedicine.medical_treatmentNudeNicotinamide phosphoribosyltransferaseApoptosisColorectal NeoplasmInbred C57BLMicechemistry.chemical_compound0302 clinical medicineTumor Cells CulturedHematopoiesiNicotinamide PhosphoribosyltransferaseInbred BALB CMice Inbred BALB CCulturedbiologySarcomaTumor CellsHaematopoiesismedicine.anatomical_structureOncology030220 oncology & carcinogenesisSirtuinFemaleSarcoma ExperimentalColorectal NeoplasmsAnimals; Apoptosis; Cell Proliferation; Colorectal Neoplasms; Female; Hematopoiesis; Humans; Mammary Neoplasms Experimental; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Mice Nude; Myeloid-Derived Suppressor Cells; NAD; Nicotinamide Phosphoribosyltransferase; Sarcoma Experimental; Signal Transduction; Tumor Cells Cultured; Xenograft Model Antitumor AssaysHumanSignal TransductionMice NudeExperimental03 medical and health sciencesmedicineMyeloid-Derived Suppressor CellAnimalsHumansCell ProliferationAnimalMyeloid-Derived Suppressor CellsMammary NeoplasmsApoptosiMammary Neoplasms ExperimentalImmunotherapyNADXenograft Model Antitumor AssaysHematopoiesisMice Inbred C57BL030104 developmental biologychemistrybiology.proteinCancer researchMyeloid-derived Suppressor CellNAD+ kinaseBone marrowCancer Research
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LC3-Associated Phagocytosis (LAP): A Potentially Influential Mediator of Efferocytosis-Related Tumor Progression and Aggressiveness

2020

One aim of cancer therapies is to induce apoptosis of tumor cells. Efficient removal of the apoptotic cells requires coordinated efforts between the processes of efferocytosis and LC3-associated phagocytosis (LAP). However, this activity has also been shown to produce anti-inflammatory and immunosuppressive signals that can be utilized by live tumor cells to evade immune defense mechanisms, resulting in tumor progression and aggressiveness. In the absence of LAP, mice exhibit suppressed tumor growth during efferocytosis, while LAP-sufficient mice show enhanced tumor progression. Little is known about how LAP or its regulators directly affect efferocytosis, tumor growth and treatment respons…

0301 basic medicineCancer ResearchPhagocytosisReviewtumor cell apoptosislcsh:RC254-28203 medical and health sciences0302 clinical medicinemedicineCytotoxic T cellEfferocytosisefferocytosistumor immune responseTumor microenvironmentbusiness.industrydigestive oral and skin physiologyCancermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensM2 macrophage activation030104 developmental biologyOncologyApoptosisTumor progression030220 oncology & carcinogenesisCancer cellLAPCancer researchbusinesshuman activitiesFrontiers in Oncology
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The secreted protein acidic and rich in cysteine is a critical mediator of cell death program induced by WIN/TRAIL combined treatment in osteosarcoma…

2015

Abstract Secreted protein acidic and rich in cysteine (SPARC) is a multi-functional protein which modulates cell-cell and cell-matrix interactions. In cancer cells, SPARC behaves as a tumor promoter in a number of tumors, but it can also act as a tumor suppressor factor. Our previous results showed that the synthetic cannabinoid WIN55,212-2 (WIN), a potent cannabinoid receptor agonist, is able to sensitize osteosarcoma MG63 cells to TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis which is accompanied with endoplasmic reticulum (ER)-stress induction and the increase in autophagic markers. In the present investigation, we studied the role of SPARC in WIN/TRAIL-induced apoptosi…

0301 basic medicineCancer ResearchProgrammed cell deathCell SurvivalMorpholinesCellSPARC cannabinoids osteosarcoma apoptosis caspase-8 activationApoptosisBone NeoplasmsBiologyNaphthalenesTNF-Related Apoptosis-Inducing Ligand03 medical and health sciences0302 clinical medicineProtein DomainsSettore BIO/10 - BiochimicaCell Line TumormedicineCytotoxic T cellHumansOsteonectinGene SilencingCaspase 8OsteosarcomaOncogeneCell DeathEndoplasmic reticulumCell MembraneCell cycleEndoplasmic Reticulum StressCell biologyBenzoxazines030104 developmental biologymedicine.anatomical_structureOncologyApoptosis030220 oncology & carcinogenesisCancer cellRNA InterferenceInternational journal of oncology
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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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Comparative analysis of the effects of a sphingosine kinase inhibitor to temozolomide and radiation treatment on glioblastoma cell lines.

2017

ABSTRACT Glioblastoma multiforme (GBM) exhibits high resistance to the standard treatment of temozolomide (TMZ) combined with radiotherapy, due to its remarkable cell heterogeneity. Accordingly, there is a need to target alternative molecules enhancing specific GBM autocrine or paracrine mechanisms and amplifying the effect of standard treatment. Sphingosine 1-phosphate (S1P) is such a lipid target molecule with an important role in cell invasion and proliferation. Sphingosine kinase inhibitors (SKI) prevent S1P formation and induce increased production of reactive oxygen species (ROS), which may potentiate radiation cytotoxicity. We analyzed the effect of SKI singular versus combined treat…

0301 basic medicineCancer ResearchRadiation-Sensitizing AgentsCell SurvivalCellSphingosine kinaseApoptosistemozolomideBiologyRadiation Tolerancesphingosine kinase inhibition03 medical and health scienceschemistry.chemical_compoundCell Line TumorX-raysmedicineHumansGPx1oxidative stressCytotoxicityAutocrine signallingAntineoplastic Agents AlkylatingPharmacologychemistry.chemical_classificationReactive oxygen speciesTemozolomideSphingosineBrain NeoplasmsDrug SynergismChemoradiotherapyMolecular biologyDacarbazinePhosphotransferases (Alcohol Group Acceptor)030104 developmental biologymedicine.anatomical_structureOncologychemistryCell cultureradiosensitivityCancer researchMolecular MedicineDrug Screening Assays AntitumorGlioblastomamedicine.drugResearch PaperCancer biologytherapy
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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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Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

2017

Abstract Thyroid carcinoma is generally associated with good prognosis, but no effective treatments are currently available for aggressive forms not cured by standard therapy. To find novel therapeutic targets for this tumor type, we had previously performed a siRNA-based functional screening to identify genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same extent for the viability of normal cells (non-oncogene addiction paradigm). Among those, we found the coatomer protein complex ζ1 (COPZ1) gene, which is involved in intracellular traffic, autophagy and lipid homeostasis. In this paper, we investigated the mechanisms through which COPZ…

0301 basic medicineCancer ResearchTime FactorsCOPZ1ApoptosisCOPZ1Thyroid cancerThyroid NeoplasmThyroidRNAi TherapeuticCell death; COPZ1; Non-oncogene addiction; Thyroid carcinoma; Animals; Apoptosis; Autophagy; Cell Line Tumor; Cell Survival; Coatomer Protein; Endoplasmic Reticulum Stress; Female; Gene Expression Regulation Neoplastic; Humans; Mice Nude; RNA Interference; Signal Transduction; Thyroid Neoplasms; Time Factors; Transfection; Tumor Burden; Unfolded Protein Response; Xenograft Model Antitumor Assays; RNAi Therapeutics; Oncology; Cancer ResearchEndoplasmic Reticulum StressOncogene AddictionTumor BurdenGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyFemaleRNA InterferenceNon-oncogene addictionHumanSignal TransductionCell deathProgrammed cell deathXenograft Model Antitumor AssayTime FactorCell SurvivalMice NudeBiologyTransfectionCoatomer ProteinThyroid carcinomaThyroid carcinoma03 medical and health sciencesCell Line TumorAutophagymedicineAnimalsHumansThyroid NeoplasmsEndoplasmic Reticulum StreAnimalAutophagyApoptosimedicine.diseaseXenograft Model Antitumor AssaysRNAi Therapeutics030104 developmental biologyImmunologyUnfolded Protein ResponseCancer researchUnfolded protein response
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Artesunate Inhibits Growth of Sunitinib-Resistant Renal Cell Carcinoma Cells through Cell Cycle Arrest and Induction of Ferroptosis

2020

Although innovative therapeutic concepts have led to better treatment of advanced renal cell carcinoma (RCC), efficacy is still limited due to the tumor developing resistance to applied drugs. Artesunate (ART) has demonstrated anti-tumor effects in different tumor entities. This study was designed to investigate the impact of ART (1&ndash

0301 basic medicineCancer ResearchTraditional Chinese Medicine (TCM) growth inhibition ferroptosis reactive oxygen species (ROS)Cell cycle checkpointBiologyurologic and male genital diseasesreactive oxygen species (ROS)lcsh:RC254-282Articlegrowth inhibition03 medical and health scienceschemistry.chemical_compound0302 clinical medicinerenal cell carcinoma (RCC)medicineClonogenic assayCytotoxicityartesunate (ART)SunitinibTraditional Chinese Medicine (TCM)Cell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensferroptosissunitib resistance030104 developmental biologyOncologychemistryCell cultureApoptosis030220 oncology & carcinogenesisCancer researchGrowth inhibitionmedicine.drugCancers
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Inhibition of colon cancer growth by docosahexaenoic acid involves autocrine production of TNFα

2016

IF 7.932; International audience; The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) has anti-inflammatory and anti-cancer properties. Among pro-inflammatory mediators, tumor necrosis factor a (TNF alpha) plays a paradoxical role in cancer biology with induction of cancer cell death or survival depending on the cellular context. The objective of the study was to evaluate the role of TNFa in DHA-mediated tumor growth inhibition and colon cancer cell death. The treatment of human colorectal cancer cells, HCT-116 and HCT-8 cells, with DHA triggered apoptosis in autocrine TNF alpha-dependent manner. We demonstrated that DHA-induced increased content of TNF alpha mRNA occurred thr…

0301 basic medicineCancer ResearchTumoricidal ActionApoptosis[ SDV.CAN ] Life Sciences [q-bio]/CancerMice[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsForkhead Box Protein O3Cell cycle3. Good healthCell biologyGene Expression Regulation NeoplasticAutocrine CommunicationColonic NeoplasmsTumor-Necrosis-FactorTumor necrosis factor alphaProgrammed cell deathDocosahexaenoic AcidsHuman Colorectal-CancerGene-Expression[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesGrowth factor receptorLipid-MetabolismGeneticsmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCell-DeathPolyunsaturated Fatty-AcidsAutocrine signallingMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyActivated Protein-KinaseTumor Necrosis Factor-alpha[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyInduced ApoptosisCancerHCT116 Cellsmedicine.diseaseXenograft Model Antitumor AssaysMicroRNAs030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsApoptosisCancer cellCancer researchPrevents Breast-Cancer
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