0000000000141401

AUTHOR

Silvia Volpe

showing 5 related works from this author

p63 Isoforms Regulate Metabolism of Cancer Stem Cells

2014

p63 is an important regulator of epithelial development expressed in different variants containing (TA) or lacking (ΔN) the N-terminal transactivation domain. The different isoforms regulate stem-cell renewal and differentiation as well as cell senescence. Several studies indicate that p63 isoforms also play a role in cancer development; however, very little is known about the role played by p63 in regulating the cancer stem phenotype. Here we investigate the cellular signals regulated by TAp63 and ΔNp63 in a model of epithelial cancer stem cells. To this end, we used colon cancer stem cells, overexpressing either TAp63 or ΔNp63 isoforms, to carry out a proteomic study by chemical-labeling …

Gene isoformProteomicsProteomeRegulatorBiologyProteomicsBiochemistryTransactivationCancer stem cellmedicineHumansMetabolomicsProtein IsoformsProtein Interaction MapsSettore BIO/10 - BIOCHIMICAp63 colon cancer stem cells proteomics stable isotope dimethyl labeling glucose metabolismSettore BIO/12Tumor Suppressor ProteinsCancerGeneral Chemistrymedicine.diseasePhenotypePeptide FragmentsCell biologyIsotope LabelingNeoplastic Stem CellsStem cellSignal TransductionTranscription Factors
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miR-205-5p-mediated downregulation of ErbB/HER receptors in breast cancer stem cells results in targeted therapy resistance

2015

AbstractThe ErbB tyrosine kinase receptor family has been shown to have an important role in tumorigenesis, and the expression of its receptor members is frequently deregulated in many types of solid tumors. Various drugs targeting these receptors have been approved for cancer treatment. Particularly, in breast cancer, anti-Her2/EGFR molecules represent the standard therapy for Her2-positive malignancies. However, in a number of cases, the tumor relapses or progresses thus suggesting that not all cancer cells have been targeted. One possibility is that a subset of cells capable of regenerating the tumor, such as cancer stem cells (CSCs), may not respond to these therapeutic agents. Accumula…

P63cancer stem cellsCancer ResearchReceptor ErbB-2oncogenesmedicine.medical_treatmentmedicine.disease_causeTargeted therapyERBB3Molecular Targeted TherapyDEATHErbB ReceptorsGene Expression Regulation NeoplasticNeoplastic Stem CellsFemaleOriginal Articlemedicine.drugCARCINOMAMIGRATIONCancer Stem Cells; Breast CancerImmunologyBreast NeoplasmsCancer Stem CellMIR-205miR-205-5pBiologyLapatinibcancer treatmentNOCellular and Molecular Neurosciencebreast cancerBreast cancerErbBCancer stem cellCell Line TumormedicineHumansSUPPRESSIONCell ProliferationMESENCHYMAL TRANSITIONtumorigenesis cancer treatment cancer stem cells miR-205-5p oncogenes breast cancerMICRORNA EXPRESSIONTumor Suppressor ProteinsLapatinibCell BiologyTrastuzumabmedicine.diseaseGENEMicroRNAstumorigenesisDrug Resistance NeoplasmCancer cellQuinazolinesCancer researchNeoplasm Recurrence LocalCarcinogenesisTranscription FactorsCell Death & Disease
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CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.

2014

SummaryCancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6− progenitor cells do not give rise to metastatic lesions but, when…

CA15-3Animals; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Hyaluronan Receptors; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Molecular Medicine; Genetics; Cell BiologyCarcinogenesisWnt ProteinMice SCIDmedicine.disease_causeAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular ReprogrammingMetastasisMicePhosphatidylinositol 3-KinasesCD44Neoplasm MetastasisCarcinogenesiPhosphoinositide-3 Kinase InhibitorsColonic NeoplasmTumorbiologyProto-Oncogene Proteins c-metCellular ReprogrammingPrognosisAntigens CD44Neoplasm ProteinsNeoplasm MetastasiAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Cell Biology; Molecular Medicine; GeneticsHyaluronan ReceptorsTreatment OutcomeBone Morphogenetic ProteinsColonic NeoplasmsNeoplastic Stem CellsFibroblastMolecular MedicineHepatocyte growth factorStem cellHumanmedicine.drugSignal TransductionPrognosiProtein Kinase InhibitorSCIDNeoplasm ProteinCancer stem cellSettore MED/04 - PATOLOGIA GENERALEmedicineGeneticsBiomarkers TumorAnimalsHumansAntigensProgenitor cellProtein Kinase InhibitorsSettore MED/04 - Patologia GeneraleAnimalBone Morphogenetic Proteincancer metastasisCD44Cell BiologyFibroblastsmedicine.diseaseWnt ProteinsSettore MED/18 - Chirurgia GeneraleImmunologyCancer researchbiology.proteinNeoplastic Stem CellPhosphatidylinositol 3-KinaseCarcinogenesisBiomarkersCell stem cell
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ErbB-3 activation by NRG-1β sustains growth and promotes vemurafenib resistance in BRAF-V600E colon cancer stem cells (CSCs)

2015

Approximately 5-10% of metastatic colorectal cancers harbor a BRAF-V600E mutation, which is correlated with resistance to EGFR-targeted therapies and worse clinical outcome. Vice versa, targeted inhibition of BRAF-V600E with the selective inhibitor PLX 4032 (Vemurafenib) is severely limited due to feedback re-activation of EGFR in these tumors. Mounting evidence indicates that upregulation of the ErbB-3 signaling axis may occur in response to several targeted therapeutics, including Vemurafenib, and NRG-1β-dependent re-activation of the PI3K/AKT survival pathway has been associated with therapy resistance. Here we show that colon CSCs express, next to EGFR and ErbB-2, also significant amoun…

Proto-Oncogene Proteins B-rafMAPK/ERK pathwayIndolesReceptor ErbB-3Colorectal cancerNeuregulin-1colon cancer stem cellsMice NudeAntineoplastic AgentsMiceErbBErbB-3medicineAnimalsHumansNeuregulin 1VemurafenibClonogenic assayskin and connective tissue diseasesProtein kinase BneoplasmsPI3K/AKT/mTOR pathwayCell ProliferationOligonucleotide Array Sequence AnalysisNRG-1βSulfonamidesbiologyReverse Transcriptase Polymerase Chain Reactionbusiness.industryFlow Cytometrymedicine.diseaseImmunohistochemistryXenograft Model Antitumor AssaysVemurafenibOncologyDrug Resistance NeoplasmColonic NeoplasmsImmunologyNeoplastic Stem CellsCancer researchbiology.proteinbusinessPriority Research Papermedicine.drug
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Breast cancer stem cells rely on fermentative glycolysis and are sensitive to 2-deoxyglucose treatment

2014

A number of studies suggest that cancer stem cells are essential for tumour growth, and failure to target these cells can result in tumour relapse. As this population of cells has been shown to be resistant to radiation and chemotherapy, it is essential to understand their biology and identify new therapeutic approaches. Targeting cancer metabolism is a potential alternative strategy to counteract tumour growth and recurrence. Here we applied a proteomic and targeted metabolomic analysis in order to point out the main metabolic differences between breast cancer cells grown as spheres and thus enriched in cancer stem cells were compared with the same cells grown in adherent differentiating c…

Cancer ResearchImmunologyPopulationPyruvate KinaseBreast NeoplasmsOxidative phosphorylationBiologyDeoxyglucoseOxidative PhosphorylationCellular and Molecular Neurosciencechemistry.chemical_compoundPYRUVATE-KINASE M2Cancer stem cellLactate dehydrogenaseCell Line TumorHumansGlycolysiseducationSettore BIO/10 - BIOCHIMICASettore MED/04 - Patologia Generaleeducation.field_of_studyL-Lactate DehydrogenaseCell growthTUMOR-GROWTHSettore BIO/12Cell BiologyCell biologychemistry2-deoxyglucose BCSCNeoplastic Stem CellsFemaleOriginal ArticleStem cellGlycolysisPyruvate kinase
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