Search results for "epithelial–mesenchymal transition"

showing 10 items of 79 documents

The transcription factor ZEB1 (deltaEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity.

2007

Epithelial to mesenchymal transition (EMT) is implicated in the progression of primary tumours towards metastasis and is likely caused by a pathological activation of transcription factors regulating EMT in embryonic development. To analyse EMT-causing pathways in tumouri-genesis, we identified transcriptional targets of the E-cadherin repressor ZEB1 in invasive human cancer cells. We show that ZEB1 repressed multiple key determinants of epithelial differentiation and cell–cell adhesion, including the cell polarity genes Crumbs3, HUGL2 and Pals1-associated tight junction protein. ZEB1 associated with their endogenous promoters in vivo, and strongly repressed promotor activities in reporter …

AdultCancer ResearchChromatin ImmunoprecipitationCellular differentiationImmunoblottingDown-RegulationBreast NeoplasmsBiologymedicine.disease_causeEpitheliumArticleCell polarityGeneticsmedicineTumor Cells CulturedHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionCell adhesionPromoter Regions GeneticMolecular BiologyTranscription factorEpithelial polarityAgedOligonucleotide Array Sequence AnalysisHomeodomain ProteinsMembrane GlycoproteinsReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell PolarityMembrane ProteinsZinc Finger E-box-Binding Homeobox 1Cell DifferentiationMiddle AgedCadherinsCytoskeletal ProteinsMicroscopy FluorescenceCancer cellColonic NeoplasmsCancer researchDisease ProgressionSnail Family Transcription FactorsCarcinogenesisNucleoside-Phosphate KinaseTranscription FactorsOncogene
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EPDR1 up-regulation in human colorectal cancer is related to staging and favours cell proliferation and invasiveness

2020

The finding of novel molecular markers for prediction or prognosis of invasiveness in colorectal cancer (CRC) constitutes an appealing challenge. Here we show the up-regulation of EPDR1 in a prospective cohort of 101 CRC patients, in a cDNA array of 43 patients and in in silico analyses. EPDR1 encodes a protein related to ependymins, a family of glycoproteins involved in intercellular contacts. A thorough statistical model allowed us to conclude that the gene is significantly up-regulated in tumour tissues when compared with normal mucosa. These results agree with those obtained by the analysis of three publicly available databases. EPDR1 up-regulation correlates with the TNM staging parame…

AdultMale0301 basic medicineEpithelial-Mesenchymal TransitionColorectal cancerIn silicolcsh:MedicineNerve Tissue ProteinsBiologyArticle//purl.org/becyt/ford/3.3 [https]03 medical and health sciences0302 clinical medicinemedicinecancerHumansNeoplasm InvasivenesshumanProspective StudiesEpithelial–mesenchymal transitionlcsh:ScienceAgedCell ProliferationNeoplasm StagingcolorectalAged 80 and overRegulation of gene expressionMultidisciplinaryCell growthlcsh:RMethylationMiddle Agedmedicine.diseaseColorectal cancerNeoplasm ProteinsUp-RegulationEPDR1Gene Expression Regulation Neoplastic030104 developmental biologyCpG siteCell culture030220 oncology & carcinogenesisCancer research//purl.org/becyt/ford/3 [https]Femalelcsh:QColorectal NeoplasmsTranscriptionScientific Reports
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Gene Expression Profiling of Epithelial–Mesenchymal Transition in Primary Breast Cancer Cell Culture

2014

Background/Aim: Epithelial–mesenchymal transition (EMT) is a process co-opted by cancer cells to invade and form metastases. In the present study we analyzed gene expression profiles of primary breast cancer cells in culture in order to highlight genes related to EMT. Materials and Methods: Microarray expression analysis of primary cells isolated from a specimen of a patient with an infiltrating ductal carcinoma of the breast was performed. Real-Time Quantitative Reverse Transcription PCR (qRT-PCR) analyses validated microarray gene expression trends. Results: Thirty-six candidate genes were selected and used to generate a molecular network displaying the tight relationship among them. The …

Breast cancer primary cell culture epithelial–mesenchymal transition EMT cDNA microarray
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Abstract LB-399: Chronic inhibition of mutant EGFR in NSCLC leads to EGFR TKI resistance by TGF-β1 mediated epithelial to mesenchymal transition

2011

Abstract In NSCLC, activating EGFR mutations underlie responsiveness of NSCLCs to reversible EGFR tyrosine kinase inhibitors (TKIs), including gefitinib and erlotinib. Despite initial responses, acquired resistance invariably develops, mediated by the emergence of the secondary T790M mutation and by focal amplification of MET, in approximately 50% and 30% of patients, respectively. The resistance mechanisms for the remaining 20% of cases remain elusive. EGFR TKI-sensitive HCC827 cells were exposed to graded concentrations of erlotinib for 6 months. Approximately 70% of the isolated clones were resistant to erlotinib and harbored MET amplification, and were sensitive to dual EGFR/MET inhibit…

Cancer ResearchGene knockdownGrowth factormedicine.medical_treatmentBiologyPhenotyperespiratory tract diseasesT790MGefitinibOncologyImmunologymedicineCancer researchERBB3ErlotinibEpithelial–mesenchymal transitionmedicine.drugCancer Research
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A quest for initiating cells of head and neck cancer and their treatment.

2010

The biology of head and neck squamous cell carcinomas (HNSCC) and other cancers have been related to cancer stem-like cells (CSC). Specific markers, which vary considerably depending on tumor type or tissue of origin, characterize CSC. CSC are cancer initiating, sustaining and mostly quiescent. Compared to bulk tumors, CSC are less sensitive to chemo- and radiotherapy and may have low immunogenicity. Therapeutic targeting of CSC may improve clinical outcome. HNSCC has two main etiologies: human papillomavirus, a virus infecting epithelial stem cells, and tobacco and alcohol abuse. Here, current knowledge of HNSCC-CSC biology is reviewed and parallels to CSC of other origin are drawn where n…

Cancer ResearchPathologymedicine.medical_specialtymedicine.medical_treatmentepithelial mesenchymal transitionSox2Reviewlcsh:RC254-282NanogMetastasisstemnessSOX2RadioresistancemedicinemetastasisEpithelial–mesenchymal transitionALDH1human papillomavirusbusiness.industryHead and neck cancerCancerchemoresistancelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseOct3/4Radiation therapyradioresistancestomatognathic diseasesOncologyCancer researchimmunotherapyStem cellbusinessCancers
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Tumor and its microenvironment: a synergistic interplay.

2013

The mutual and interdependent interaction between tumor and its microenvironment is a crucial topic in cancer research. Recently, it was reported that targeting stromal events could improve efficacies of current therapeutics and prevent metastatic spreading. Tumor microenvironment is a "complex network" of different cell types, soluble factors, signaling molecules and extracellular matrix components, which orchestrate the fate of tumor progression. As by definition, cancer stem cells (CSCs) are proposed to be the unique cell type able to maintain tumor mass and survive outside the primary tumor at metastatic sites. Being exposed to environmental stressors, including reactive oxygen species …

Cancer ResearchStromal cellEpithelial-Mesenchymal TransitionAngiogenesisCell SurvivalBiologyCancer stem cellCell MovementNeoplasmsmedicineTumor MicroenvironmentAnimalsHumansEpithelial–mesenchymal transitionNeoplasm MetastasisStem Cell NicheHypoxiaTumor microenvironmentNeovascularization Pathologicmedicine.diseaseAngiogenesis CAFs CAMs CRC CSCs ECM EMT GSH HIF Hypoxia MMPs ROS Tumor microenvironment VEGF cancer stem cells cancer-associated fibroblasts cancer-associated macrophages colorectal cancer epithelial mesenchymal transition extracellular matrix hypoxia-inducible factor matrix metalloproteinase reactive oxygen species reduced glutathione vascular endothelial growth factorPrimary tumorTumor progressionImmunologyCancer researchNeoplastic Stem CellsCancer-Associated FibroblastsOxidation-ReductionSignal Transduction
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Intratumoral Heterogeneity in EGFR-Mutant NSCLC Results in Divergent Resistance Mechanisms in Response to EGFR Tyrosine Kinase Inhibition

2015

Abstract Non–small cell lung cancers (NSCLC) that have developed resistance to EGF receptor (EGFR) tyrosine kinase inhibitor (TKI), including gefitinib and erlotinib, are clinically linked to an epithelial-to-mesenchymal transition (EMT) phenotype. Here, we examined whether modulating EMT maintains the responsiveness of EGFR-mutated NSCLCs to EGFR TKI therapy. Using human NSCLC cell lines harboring mutated EGFR and a transgenic mouse model of lung cancer driven by mutant EGFR (EGFR-Del19-T790M), we demonstrate that EGFR inhibition induces TGFβ secretion followed by SMAD pathway activation, an event that promotes EMT. Chronic exposure of EGFR-mutated NSCLC cells to TGFβ was sufficient to ind…

Cancer Researchmedicine.drug_classCellBiologymedicine.diseaseArticleTyrosine-kinase inhibitorrespiratory tract diseasesmedicine.anatomical_structureGefitinibOncologyProtein kinase domainImmunologymedicineCancer researchEpithelial–mesenchymal transitionErlotinibSignal transductionLung cancerneoplasmsmedicine.drugCancer Research
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The complex interplay between Notch signaling and Snail1 transcription factor in the regulation of epithelial–mesenchymal transition (EMT)

2015

Background The epithelial–mesenchymal transition (EMT) is a highly coordinated process observed during embryonic development and adult tissue repair. It is characterized by the loss of cell–cell adhesion and apicobasal polarity, and the transition to a cell type with a spindle-like phenotype able to migrate through the basal membranes. Methods This review article includes available date from peer-reviewed publications associated with the role of Notch signaling and Snail1 transcription factor in activation and regulation of EMT. Results Growing evidences in the past few years demonstrated a significant role of Notch in EMT activation. It is not surprising because this pathway is the nexus o…

Cell typeNotchSnail1business.industryEMTNotch signaling pathwayAnatomyPhenotypeCell biologyTGFβDownregulation and upregulationCompartment (development)Mesenchymal–epithelial transitionMedicineSurgeryEpithelial–mesenchymal transitionHypoxiabusinessTranscription factorCancerEuropean Surgery
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The Epithelial Mesenchymal Transition Process in Wilms Tumor

2011

Background Until now, only a few mouse-transplanted human tumors or experimental Wilms tumor (WT) cell lines have been described. The aim of this study was to show the biological behavior, including histology, immunohistochemistry (IHC), and molecular biology, of a WT including the original tumor and metastasis transferred into nude mice and followed for successive generations in xenografts. Methods A WT metastasis was xenotransplanted into nude mice and the mice was monitored for 7 passages over a period of 29 months; the original neoplasm was comparatively studied. The morphology was evaluated by optical and electron microscopy. The protein expression was analyzed by immunohistochemistry …

Epithelial-Mesenchymal TransitionHistologyDNA Mutational AnalysisMice NudeCell Growth ProcessesWilms TumorBone and BonesPathology and Forensic MedicineMetastasisMicemedicineAnimalsHumansEpithelial–mesenchymal transitionNeoplasm MetastasisOncogene ProteinsN-Myc Proto-Oncogene ProteinTissue microarrayChemistryMesenchymal stem cellNuclear ProteinsEye Diseases HereditaryWilms' tumorHistologyStriated muscle cell differentiationMicroarray Analysismedicine.diseaseImmunohistochemistryXenograft Model Antitumor AssaysKidney NeoplasmsWnt ProteinsRadiusMedical Laboratory TechnologyMutationCancer researchImmunohistochemistrySignal TransductionApplied Immunohistochemistry & Molecular Morphology
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Key nodes of a microRNA network associated with the integrated mesenchymal subtype of high-grade serous ovarian cancer

2015

Metastasis is the main cause of cancer mortality. One of the initiating events of cancer metastasis of epithelial tumors is epithelial-to-mesenchymal transition (EMT), during which cells dedifferentiate from a relatively rigid cell structure/morphology to a flexible and changeable structure/morphology often associated with mesenchymal cells. The presence of EMT in human epithelial tumors is reflected by the increased expression of genes and levels of proteins that are preferentially present in mesenchymal cells. The combined presence of these genes forms the basis of mesenchymal gene signatures, which are the foundation for classifying a mesenchymal subtype of tumors. Indeed, tumor classifi…

Epithelial-Mesenchymal TransitionReviewBiologyBioinformaticsMetastasis03 medical and health sciences0302 clinical medicinemicroRNAGene expressionmedicineHumanscancerEpithelial–mesenchymal transitionCystadenocarcinomaGene030304 developmental biologyOvarian Neoplasms0303 health sciencesMessenger RNAmiR-506Mesenchymal stem cellmiR-101medicine.diseaseCystadenocarcinoma Serous3. Good healthMicroRNAsOncology030220 oncology & carcinogenesisCancer researchFemaleovaryMicroRNA (miRNA)epithelial-to-mesenchymal transition (EMT)Chinese Journal of Cancer
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