Search results for " STEM"

showing 10 items of 2170 documents

NOTCH3 expression is linked to breast cancer seeding and distant metastasis

2018

Background Development of distant metastases involves a complex multistep biological process termed the invasion-metastasis cascade, which includes dissemination of cancer cells from the primary tumor to secondary organs. NOTCH developmental signaling plays a critical role in promoting epithelial-to-mesenchymal transition, tumor stemness, and metastasis. Although all four NOTCH receptors show oncogenic properties, the unique role of each of these receptors in the sequential stepwise events that typify the invasion-metastasis cascade remains elusive. Methods We have established metastatic xenografts expressing high endogenous levels of NOTCH3 using estrogen receptor alpha-positive (ERα+) MCF…

0301 basic medicineCancer ResearchTransplantation HeterologousNotch signaling pathwayEstrogen receptorMice NudeBreast NeoplasmsTriple Negative Breast NeoplasmsTumor stemneCentrosome amplificationTumor stemnessMetastasilcsh:RC254-282MetastasisMetastasis03 medical and health sciences0302 clinical medicineBreast cancerNeoplasm SeedingBreast cancerSurgical oncologyCell Line TumormedicineAnimalsHumansCell Self RenewalReceptor Notch3business.industryGene Expression ProfilingMiddle Agedmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrimary tumorSurvival Analysis3. Good healthChromosomal instabilityGene Expression Regulation NeoplasticSettore BIO/18 - Genetica030104 developmental biologyOncology030220 oncology & carcinogenesisCancer cellCancer researchMCF-7 CellsFemaleRNA InterferencebusinessBrain metastasisResearch ArticleBreast Cancer Research
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Pattern of Invasion in Human Pancreatic Cancer Organoids Is Associated with Loss of SMAD4 and Clinical Outcome

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by extensive local invasion and systemic spread. In this study, we employed a three-dimensional organoid model of human pancreatic cancer to characterize the molecular alterations critical for invasion. Time-lapse microscopy was used to observe invasion in organoids from 25 surgically resected human PDAC samples in collagen I. Subsequent lentiviral modification and small-molecule inhibitors were used to investigate the molecular programs underlying invasion in PDAC organoids. When cultured in collagen I, PDAC organoids exhibited two distinct, morphologically defined invasive phenotypes, mesenchymal an…

0301 basic medicineCancer Researchendocrine system diseasesPancreatic ductal adenocarcinoma (PDAC)RAC1CDC42AdenocarcinomaBiologyArticle03 medical and health sciences0302 clinical medicineHuman Pancreatic CancerCell MovementPancreatic cancerBiomarkers TumorTumor Cells CulturedmedicineOrganoidHumansNeoplasm InvasivenessCell ProliferationSmad4 ProteinRegulation of gene expressionCell growthMesenchymal stem cellPrognosismedicine.diseasePhenotypedigestive system diseasesGene Expression Regulation NeoplasticOrganoidsPancreatic NeoplasmsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisembryonic structuresCancer researchCarcinoma Pancreatic DuctalSignal TransductionCancer Research
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Diversity of Clinically Relevant Outcomes Resulting from Hypofractionated Radiation in Human Glioma Stem Cells Mirrors Distinct Patterns of Transcrip…

2020

Hypofractionated radiotherapy is the mainstay of the current treatment for glioblastoma. However, the efficacy of radiotherapy is hindered by the high degree of radioresistance associated with glioma stem cells comprising a heterogeneous compartment of cell lineages differing in their phenotypic characteristics, molecular signatures, and biological responses to external signals. Reconstruction of radiation responses in glioma stem cells is necessary for understanding the biological and molecular determinants of glioblastoma radioresistance. To date, there is a paucity of information on the longitudinal outcomes of hypofractionated radiation in glioma stem cells. This study addresses long-te…

0301 basic medicineCancer Researchmedicine.medical_treatmentCell150610Biologylcsh:RC254-282ArticleTranscriptome03 medical and health sciences0302 clinical medicineRadioresistanceGliomamedicineCell growthglioblastomamedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPhenotypeRadiation therapyradioresistance030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchglioma stem cellsStem cellhypofractionated radiationCancers
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Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis

2019

Summary MyD88, an adaptor molecule downstream of innate pathways, plays a significant tumor-promoting role in sporadic intestinal carcinogenesis of the Apcmin/+ model, which carries a mutation in the Apc gene. Here, we show that deletion of MyD88 in intestinal mesenchymal cells (IMCs) significantly reduces tumorigenesis in this model. This phenotype is associated with decreased epithelial cell proliferation, altered inflammatory and tumorigenic immune cell infiltration, and modified gene expression similar to complete MyD88 knockout mice. Genetic deletion of TLR4, but not interleukin-1 receptor (IL-1R), in IMCs led to altered molecular profiles and reduction of intestinal tumors similar to …

0301 basic medicineCarcinogenesisBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyExtracellular matrixMice03 medical and health sciences0302 clinical medicinemedicinetumor microenvironmentAnimalsHumansReceptorinnate immunityTumor microenvironmentInnate immune systemMesenchymal stem cellCell biologyIntestinesToll-Like Receptor 4030104 developmental biologyMyeloid Differentiation Factor 88Knockout mouseTLR4Carcinogenesiscancer-associated fibroblasts030217 neurology & neurosurgerySignal Transduction
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c-Fos induces chondrogenic tumor formation in immortalized human mesenchymal progenitor cells

2018

Mesenchymal progenitor cells (MPCs) have been hypothesized as cells of origin for sarcomas, and c-Fos transcription factor has been showed to act as an oncogene in bone tumors. In this study, we show c-Fos is present in most sarcomas with chondral phenotype, while multiple other genes are related to c-Fos expression pattern. To further define the role of c-Fos in sarcomagenesis, we expressed it in primary human MPCs (hMPCs), immortalized hMPCs and transformed murine MPCs (mMPCs). In immortalized hMPCs, c-Fos expression generated morphological changes, reduced mobility capacity and impaired adipogenic- and osteogenic-differentiation potentials. Remarkably, immortalized hMPCs or mMPCs express…

0301 basic medicineCarcinogenesisCelllcsh:MedicineMice SCIDArticleCell Line03 medical and health sciencesMice0302 clinical medicineMice Inbred NODmedicineAnimalsHumansProgenitor celllcsh:ScienceRegulation of gene expressionMultidisciplinaryOncogeneChemistryMesenchymal stem celllcsh:RGenes fosMesenchymal Stem CellsSarcomaChondrogenesisPhenotypeCell biologyGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticCell culture030220 oncology & carcinogenesislcsh:QProto-Oncogene Proteins c-fos
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Mcl-1 targeting could be an intriguing perspective to cure cancer

2018

The Bcl-2 family, which plays important roles in controlling cancer development, is divided into antiapoptotic and proapoptotic members. The change in the balance between these members governs the life and death of the cells. Mcl-1 is an antiapoptotic member of this family and its distribution in normal and cancerous tissues strongly differs from that of Bcl-2. In human cancers, where upregulation of antiapoptotic proteins is common, Mcl-1 expression is regulated independent of Bcl-2 and its inhibition promotes senescence, a major barrier to tumorigenesis. Cancer chemotherapy determines various kinds of responses, such as senescence and autophagy; however, the ideal response to chemotherapy…

0301 basic medicineCarcinogenesisPhysiologyClinical BiochemistryApoptosisBiologymedicine.disease_causecancer care03 medical and health sciencesMcl-1 in cancer0302 clinical medicineBcl-2 familyimmune system diseasesCancer stem cellhemic and lymphatic diseasesNeoplasmsmedicinecancer-stem-cellHumansPost-translational regulationMolecular Targeted TherapyneoplasmsCellular SenescenceOncogeneBcl-2 familyAutophagyCancerCell Biologymedicine.diseaseMcl-1 isoformGene Expression Regulation Neoplastic030104 developmental biologyUSP9XProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCancer researchtargeting Mcl-1Myeloid Cell Leukemia Sequence 1 ProteinCarcinogenesisProtein Processing Post-Translational
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Inflammatory Response Mechanisms of the Dentine–Pulp Complex and the Periapical Tissues

2021

The macroscopic and microscopic anatomy of the oral cavity is complex and unique in the human body. Soft-tissue structures are in close interaction with mineralized bone, but also dentine, cementum and enamel of our teeth. These are exposed to intense mechanical and chemical stress as well as to dense microbiologic colonization. Teeth are susceptible to damage, most commonly to caries, where microorganisms from the oral cavity degrade the mineralized tissues of enamel and dentine and invade the soft connective tissue at the core, the dental pulp. However, the pulp is well-equipped to sense and fend off bacteria and their products and mounts various and intricate defense mechanisms. The fron…

0301 basic medicineCarcinogenesisRoot canalReviewimmune responselcsh:Chemistryodontoblast0302 clinical medicinePulpitislcsh:QH301-705.5SpectroscopyTissue homeostasisOdontoblastsPeriapical TissueIntracellular Signaling Peptides and ProteinsGeneral MedicineComputer Science ApplicationsCell biologyPeriradicularmedicine.anatomical_structureCarcinoma Squamous CellMouth NeoplasmsChemokinescarious lesionPeriapical GranulomaConnective tissueDental CariesBiologyNitric OxideCatalysisInorganic Chemistry03 medical and health sciencestertiary dentinestomatognathic systemAntigens NeoplasmmedicineAnimalsHumansddc:610Physical and Theoretical ChemistryApical foramenMolecular BiologyDental PulpRadicular CystNeuropeptidesOrganic ChemistryPulpitisMesenchymal Stem CellsComplement System Proteins030206 dentistryFibroblastsmedicine.diseasestomatognathic diseases030104 developmental biologyOdontoblastlcsh:Biology (General)lcsh:QD1-999DentinPulp (tooth)Nerve NetPeriapical PeriodontitisInternational Journal of Molecular Sciences
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MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
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Induction of cancer cell stemness by depletion of macrohistone H2A1 in hepatocellular carcinoma.

2017

Hepatocellular carcinomas (HCC) contain a subpopulation of cancer stem cells (CSCs), which exhibit stem cell–like features and are responsible for tumor relapse, metastasis, and chemoresistance. The development of effective treatments for HCC will depend on a molecular-level understanding of the specific pathways driving CSC emergence and stemness. MacroH2A1 is a variant of the histone H2A and an epigenetic regulator of stem-cell function, where it promotes differentiation and, conversely, acts as a barrier to somatic-cell reprogramming. Here, we focused on the role played by the histone variant macroH2A1 as a potential epigenetic factor promoting CSC differentiation. In human HCC section…

0301 basic medicineCarcinoma HepatocellularBiologyMetastasisHistones03 medical and health sciencesCancer stem cellHistone H2AmedicineHumansEpigeneticsPhosphorylationCell ProliferationHepatologyCell growthGene Expression ProfilingLiver NeoplasmsTranscription Factor RelAHep G2 Cellsmedicine.disease030104 developmental biologyHistoneCancer cellCancer researchbiology.proteinNeoplastic Stem CellsReprogrammingHepatology (Baltimore, Md.)
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Extracellular histones activate autophagy and apoptosis via mTOR signaling in human endothelial cells.

2018

Circulating histones have been proposed as targets for therapy in sepsis and hyperinflammatory symptoms. However, the proposed strategies have failed in clinical trials. Although different mechanisms for histone-related cytotoxicity are being explored, those mediated by circulating histones are not fully understood. Extracellular histones induce endothelial cell death, thereby contributing to the pathogenesis of complex diseases such as sepsis and septic shock. Therefore, the comprehension of cellular responses triggered by histones is capital to design effective therapeutic strategies. Here we report how extracellular histones induce autophagy and apoptosis in a dose-dependent manner in cu…

0301 basic medicineCell SurvivalEndothelial cellsFisiologiaApoptosisAMP-Activated Protein KinasesHistones03 medical and health sciencesExtracellularAutophagyHuman Umbilical Vein Endothelial CellsAutophagy-Related Protein-1 HomologHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologyDose-Response Relationship DrugChemistryTOR Serine-Threonine KinasesAutophagyIntracellular Signaling Peptides and ProteinsAMPKNuclear ProteinsCirculating histonesCell biologyToll-like receptorsEndothelial stem cell030104 developmental biologyHistoneApoptosisbiology.proteinMolecular MedicineProto-Oncogene Proteins c-aktSignal TransductionBiochimica et biophysica acta. Molecular basis of disease
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