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showing 10 items of 10255 documents

IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

2017

Abstract The tumor microenvironment supplies proinflammatory cytokines favoring a permissive milieu for cancer cell growth and invasive behavior. Here we show how breast cancer progression is facilitated by IL4 secreted by adipose tissue and estrogen receptor–positive and triple-negative breast cancer cell types. Blocking autocrine and paracrine IL4 signaling with the IL4Rα antagonist IL4DM compromised breast cancer cell proliferation, invasion, and tumor growth by downregulating MAPK pathway activity. IL4DM reduced numbers of CD44+/CD24− cancer stem-like cells and elevated expression of the dual specificity phosphatase DUSP4 by inhibiting NF-κB. Enforced expression of DUSP4 drove conversio…

0301 basic medicineCancer ResearchBlotting WesternCA 15-3Breast Neoplasms03 medical and health sciencesParacrine signalling0302 clinical medicineBreast cancerCell Line TumorTumor MicroenvironmentmedicineHumansskin and connective tissue diseasesAutocrine signallingDual-Specificity PhosphataseBlotting Western; Breast Neoplasms; Cell Line Tumor; Disease Progression; Dual-Specificity Phosphatases; Female; Flow Cytometry; Heterografts; Humans; Interleukin-4; Mitogen-Activated Protein Kinase Phosphatases; Tumor Microenvironment; Oncology; Cancer ResearchTumor microenvironmentbiologyCD44CancerFlow Cytometrymedicine.disease030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer cellDisease Progressionbiology.proteinCancer researchDual-Specificity PhosphatasesHeterograftsMitogen-Activated Protein Kinase PhosphatasesFemaleInterleukin-4HeterograftMitogen-Activated Protein Kinase PhosphataseBreast NeoplasmHumanCancer Research
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Thymic Hyperplasia with Lymphoepithelial Sialadenitis (LESA)-Like Features: Strong Association with Lymphomas and Non-Myasthenic Autoimmune Diseases.

2021

Thymic hyperplasia (TH) with lymphoepithelial sialadenitis (LESA)-like features (LESA-like TH) has been described as a tumor-like, benign proliferation of thymic epithelial cells and lymphoid follicles. We aimed to determine the frequency of lymphoma and autoimmunity in LESA-like TH and performed retrospective analysis of cases with LESA-like TH and/or thymic MALT-lymphoma. Among 36 patients (21 males) with LESA-like TH (age 52 years, 32&ndash

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyPure red cell aplasia610 Medicine & healthautoimmune diseaselymphomathymitismedicine.disease_causelcsh:RC254-282SclerodermaArticleAutoimmunitysurgery03 medical and health sciences0302 clinical medicinethymusimmune system diseaseshemic and lymphatic diseasesmedicineddc:610Autoimmune diseasebusiness.industryLESAimagingHyperplasialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseLESA; autoimmune disease; imaging; lymphoma; myasthenia; pathology; surgery; thymic epithelial tumor; thymitis; thymusSialadenitisMyasthenia gravis3. Good healthLymphomamyasthenia030104 developmental biologyOncologythymic epithelial tumor030220 oncology & carcinogenesis570 Life sciences; biologypathologybusiness
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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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Epigenetic Silencing of CDR1as Drives IGF2BP3-Mediated Melanoma Invasion and Metastasis.

2018

Summary Metastasis is the primary cause of death of cancer patients. Dissecting mechanisms governing metastatic spread may uncover important tumor biology and/or yield promising therapeutic insights. Here, we investigated the role of circular RNAs (circRNA) in metastasis, using melanoma as a model aggressive tumor. We identified silencing of cerebellar degeneration-related 1 antisense (CDR1as), a regulator of miR-7, as a hallmark of melanoma progression. CDR1as depletion results from epigenetic silencing of LINC00632, its originating long non-coding RNA (lncRNA) and promotes invasion in vitro and metastasis in vivo through a miR-7-independent, IGF2BP3-mediated mechanism. Moreover, CDR1as le…

0301 basic medicineCancer ResearchRegulatorNerve Tissue ProteinsBiologyAutoantigensArticleMetastasisEpigenesis Genetic03 medical and health sciences0302 clinical medicinemedicineGene silencingHumansEnhancer of Zeste Homolog 2 ProteinNeoplasm InvasivenessRNA AntisenseGene SilencingNeoplasm MetastasisMelanomaMelanomaEZH2RNACancerRNA-Binding ProteinsRNA Circularmedicine.diseasePhospholipid Hydroperoxide Glutathione PeroxidasePrognosisMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchbiology.proteinRNA Long NoncodingPRC2Cancer cell
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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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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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Hypoxia-Inducible Factor-1α Activity as a Switch for Glioblastoma Responsiveness to Temozolomide

2018

Rationale: The activity of the transcription factor, hypoxia-inducible factor (HIF)-1?, is a common driver of a number of the pathways involved in the aggressiveness of glioblastomas (GBMs), and it has been suggested that the reduction in this activity observed, soon after the administration of temozolomide (TMZ), can be a biomarker of an early response in GBM models. As HIF-1? is a tightly regulated protein, studying the processes involved in its downregulation could shed new light on the mechanisms underlying GBM sensitivity or resistance to TMZ. Methods: The effect of HIF-1? silencing on cell responsiveness to TMZ was assessed in four genetically different human GBM cell lines by evaluat…

0301 basic medicineCancer Researchapoptosis; chaperone-mediated autophagy activity; hypoxia-inducible factor-1? silencing; temozolomide responsiveness; theranostic biomarkerBiologylcsh:RC254-28203 medical and health scienceshypoxia-inducible factor-1α silencing0302 clinical medicineGliomamedicineGene silencingViability assayTranscription factorOriginal Researchchaperone-mediated autophagy activityTemozolomideAutophagyapoptosismedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenstheranostic biomarker030104 developmental biologyHypoxia-inducible factorsOncologyApoptosis030220 oncology & carcinogenesisCancer researchtemozolomide responsivenessmedicine.drugFrontiers in Oncology
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Targeting Immune Modulators in Glioma While Avoiding Autoimmune Conditions

2021

Simple Summary Glioblastoma multiforme is a futile disease usually leading to the patient’s death within one year post-diagnosis; therefore, novel treatment options are desperately needed. In this regard, activation of the inert immune system has moved into focus in recent years. Malignant brain tumors, as well as autoimmune diseases, elicit aberrant immune responses. In this way, glioma escapes the host’s immune system and, thus, activation of the immune response in order to reduce tumor tolerance can serve as an alternative treatment option. Immune checkpoint modulators in combination with traditional therapies have gained attention in both glioma and autoimmune diseases. In this review, …

0301 basic medicineCancer Researchautoimmune disease ; immune checkpoints ; immunotherapy ; clinical trials ; Gliom ; gliomamedicine.medical_treatmentautoimmune diseaseContext (language use)Review03 medical and health sciences0302 clinical medicineImmune systemgliomaGliomamedicineRC254-282Autoimmune diseaseclinical trialsTumor microenvironmentbusiness.industryMultiple sclerosisNeoplasms. Tumors. Oncology. Including cancer and carcinogensImmunosuppressionImmunotherapybiochemical phenomena metabolism and nutritionimmune checkpointsmedicine.disease030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchimmunotherapybusinessCancers
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Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis

2019

Cachexia is a debilitating syndrome that complicates the management of cancer patients. Muscle wasting, one of the main features of cachexia, is associated with hyper-activation of protein degradative pathways and altered mitochondrial function that could both result from impaired redox homeostasis. This study aimed to investigate the contribution of oxidative stress to cancer-induced cachexia in the presence or in the absence of moderate exercise training. Mice bearing the colon C26 carcinoma, either sedentary or exercised, were used. The former showed muscle wasting and redox imbalance, with the activation of an antioxidant response and with upregulation of markers of proteasome-dependent…

0301 basic medicineCancer Researchmedicine.medical_specialtyMitochondrionProtein degradationmedicine.disease_causelcsh:RC254-282ArticleMuscle wastingCachexia03 medical and health sciences0302 clinical medicineInternal medicineMitophagyAutophagymedicineChemotherapyWastingchemistry.chemical_classificationReactive oxygen speciesbusiness.industryAutophagylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseAutophagy; Chemotherapy; Mitochondria; Muscle wasting; Oxidative stress; Oncology; Cancer ResearchMitochondria030104 developmental biologyEndocrinologyOncologychemistryOxidative stress030220 oncology & carcinogenesismedicine.symptombusinessOxidative stressCancers
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Ligand-dependent Hedgehog pathway activation in Rhabdomyosarcoma : the oncogenic role of the ligands

2017

Altres ajuts: This work was supported by grants from Institut Català d'Oncologia (ICO), Instituto de Salud Carlos III (RTICC-RD12/0036/0016, /0020, /0035, /0057; and PI14/00647), Fundació A BOSCH, Fundació Amics Joan Petit, ajuts predoctorals del VHIR and RIS3CAT grants COMRDI15-1-0014 (ACCIÓ and FEDER). Altres ajuts: FEDER/COMRDI15-1-0014 Rhabdomyosarcoma (RMS) is the most common type of soft tissue sarcoma in children. The Hedgehog (HH) pathway is known to develop an oncogenic role in RMS. However, the molecular mechanism that drives activation of the pathway in RMS is not well understood. The expression of HH ligands was studied by qPCR, western blot and immunohistochemistry. Functional …

0301 basic medicineCancer ResearchsarcomaCarcinogenesisVismodegibRhabdomyosarcoma; Hedgehog; vismodegib; UPR; TRIB3; sarcoma; cancerVismodegib610ApoptosisMice SCIDUPRLigandsMice03 medical and health sciences0302 clinical medicineCell MovementvismodegibRhabdomyosarcomaTumor Cells CulturedmedicinecancerAnimalsHumansHedgehog ProteinsAutocrine signallingRhabdomyosarcomaHedgehogCell ProliferationCancerChemistryTRIB3Sarcomamedicine.diseaseXenograft Model Antitumor AssaysHedgehog signaling pathway3. Good health030104 developmental biologyOncology030220 oncology & carcinogenesisUnfolded protein responseCancer researchFemaleSignal transductionTranslational TherapeuticsSmoothenedHedgehogSignal TransductionTranscription Factorsmedicine.drug
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