0000000000354355

AUTHOR

Cosmo Rossi

showing 3 related works from this author

MiR-205-5p inhibition by locked nucleic acids impairs metastatic potential of breast cancer cells.

2018

AbstractMir-205 plays an important role in epithelial biogenesis and in mammary gland development but its role in cancer still remains controversial depending on the specific cellular context and target genes. We have previously reported that miR-205-5p is upregulated in breast cancer stem cells targeting ERBB pathway and leading to targeted therapy resistance. Here we show that miR-205-5p regulates tumorigenic properties of breast cancer cells, as well as epithelial to mesenchymal transition. Silencing this miRNA in breast cancer results in reduced tumor growth and metastatic spreading in mouse models. Moreover, we show that miR-205-5p knock-down can be obtained with the use of specific lo…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal Transitionmedicine.medical_treatmentAntagomirSettore MED/50 - Scienze Tecniche Mediche ApplicateImmunologyTransplantation HeterologousOligonucleotidesBreast NeoplasmsBiologyArticleTargeted therapy03 medical and health sciencesCellular and Molecular NeuroscienceMiceBreast cancerErbBCell MovementMice Inbred NODOligonucleotideCell Line TumormicroRNAmedicineGene silencingAnimalsHumansEpithelial–mesenchymal transitionlcsh:QH573-671Neoplasm MetastasisCell ProliferationAnimallcsh:CytologyCancerAntagomirsMicroRNACell Biologymedicine.diseaseNeoplasm MetastasiMicroRNAs030104 developmental biologyCancer researchFemaleStem cellBreast NeoplasmHumanCell deathdisease
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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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