2023
Intrahepatic Cholangiocarcinoma Developing in Patients with Metabolic Syndrome Is Characterized by Osteopontin Overexpression in the Tumor Stroma
Cadamuro M, Sarcognato S, Camerotto R, Girardi N, Lasagni A, Zanus G, Cillo U, Gringeri E, Morana G, Strazzabosco M, Campello E, Simioni P, Guido M, Fabris L. Intrahepatic Cholangiocarcinoma Developing in Patients with Metabolic Syndrome Is Characterized by Osteopontin Overexpression in the Tumor Stroma. International Journal Of Molecular Sciences 2023, 24: 4748. PMID: 36902188, PMCID: PMC10003180, DOI: 10.3390/ijms24054748.Peer-Reviewed Original ResearchConceptsMetS patientsMetabolic syndromeNon-alcoholic fatty liver disease/non-alcoholic steatohepatitisNon-alcoholic steatohepatitisIntrahepatic cholangiocarcinoma developmentPutative therapeutic targetDeposition of osteopontinCell-like phenotypeBiliary tumorigenesisExtracellular matrix depositionVascular complicationsSurgical resectionIntrahepatic cholangiocarcinomaICCA cellsOverexpression of osteopontinPredictive biomarkersLiver tumorsCommon conditionHuCCT-1Tumor stromaCholangiocarcinoma developmentPeritumoral areaTherapeutic targetBiliary differentiationOsteopontin overexpression
2019
Chronic Exposure to Chewing Tobacco Induces Metabolic Reprogramming and Cancer Stem Cell-Like Properties in Esophageal Epithelial Cells
Datta KK, Patil S, Patel K, Babu N, Raja R, Nanjappa V, Mangalaparthi KK, Dhaka B, Rajagopalan P, Deolankar SC, Kannan R, Kumar P, Prasad TSK, Mathur PP, Kumari A, Manoharan M, Coral K, Murugan S, Sidransky D, Gupta R, Gupta R, Khanna-Gupta A, Chatterjee A, Gowda H. Chronic Exposure to Chewing Tobacco Induces Metabolic Reprogramming and Cancer Stem Cell-Like Properties in Esophageal Epithelial Cells. Cells 2019, 8: 949. PMID: 31438645, PMCID: PMC6770059, DOI: 10.3390/cells8090949.Peer-Reviewed Original ResearchConceptsEsophageal epithelial cellsQuantitative proteomic analysisQuantitative proteomic profilingEpithelial cellsCancer stem cell-like phenotypeElectron transport chainEsophageal squamous cell carcinomaStem cell-like phenotypeTricarboxylic acid cycleMolecular alterationsMitochondrial proteinsTobacco exposurePhosphorylation phenotypeProteomic analysisCell-like phenotypeStem cell-like propertiesMetabolic reprogrammingProteomic profilingCancer stem cell-like propertiesOXPHOS phenotypeStem cell markersChronic exposureTransport chainCell-like propertiesMolecular markers
2018
Depletion of S100A4+ stromal cells does not prevent HCC development but reduces the stem cell-like phenotype of the tumors
Jiao J, González Á, Stevenson H, Gagea M, Sugimoto H, Kalluri R, Beretta L. Depletion of S100A4+ stromal cells does not prevent HCC development but reduces the stem cell-like phenotype of the tumors. Experimental & Molecular Medicine 2018, 50: e422-e422. PMID: 29303514, PMCID: PMC5992984, DOI: 10.1038/emm.2017.175.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinoma, HepatocellularCell DifferentiationGene Expression Regulation, NeoplasticHepatitisHepatocytesLiver NeoplasmsLiver Neoplasms, ExperimentalMice, KnockoutMice, TransgenicNeoplastic Stem CellsNon-alcoholic Fatty Liver DiseasePTEN PhosphohydrolaseS100 Calcium-Binding Protein A4Stromal CellsConceptsDepletion of S100A4Hepatocellular carcinomaMouse modelCalcium-binding protein S100A4Stromal cellsStemness phenotypeDevelopment of HCCOval cell hyperplasiaReduction of inflammationStemness propertiesCell stemness propertiesNew mouse modelStem cell-like phenotypeViral thymidine kinaseCell-like phenotypeLiver diseaseCell hyperplasiaPoor prognosisGanciclovir injectionsNAS scoreAdjacent liverGastric cancerHCC developmentProtein S100A4Hepatic deletion
2015
Leukemia inhibitory factor protects cholangiocarcinoma cells from drug-induced apoptosis via a PI3K/AKT-dependent Mcl-1 activation
Morton SD, Cadamuro M, Brivio S, Vismara M, Stecca T, Massani M, Bassi N, Furlanetto A, Joplin RE, Floreani A, Fabris L, Strazzabosco M. Leukemia inhibitory factor protects cholangiocarcinoma cells from drug-induced apoptosis via a PI3K/AKT-dependent Mcl-1 activation. Oncotarget 2015, 6: 26052-26064. PMID: 26296968, PMCID: PMC4694885, DOI: 10.18632/oncotarget.4482.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsApoptosisBile Duct NeoplasmsBlotting, WesternCell Line, TumorCholangiocarcinomaCisplatinDeoxycytidineGemcitabineGene Expression Regulation, NeoplasticHumansLeukemia Inhibitory FactorLeukemia Inhibitory Factor Receptor alpha SubunitMicroscopy, FluorescenceMyeloid Cell Leukemia Sequence 1 ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReverse Transcriptase Polymerase Chain ReactionRNA InterferenceSignal TransductionConceptsLeukemia inhibitory factorDrug-induced apoptosisChemotherapy-induced apoptosisPI3K inhibitionLIF effectsLIFR expressionExpression of LIFInhibitory factorRole of LIFCholangiocarcinoma cellsK inhibitionPI3K/Akt-dependent pathwayTumor stromal cellsHuman cholangiocarcinoma cell linesCell-like phenotypeCholangiocarcinoma cell linesMcl-1Akt-dependent pathwayUp-regulating Mcl-1IL-6 family cytokinesLIF secretionLiver malignanciesCholangiocarcinoma cell proliferationAnti-apoptotic proteinsFamily cytokines
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