2016
Low-Dose Paclitaxel Reduces S100A4 Nuclear Import to Inhibit Invasion and Hematogenous Metastasis of Cholangiocarcinoma
Cadamuro M, Spagnuolo G, Sambado L, Indraccolo S, Nardo G, Rosato A, Brivio S, Caslini C, Stecca T, Massani M, Bassi N, Novelli E, Spirli C, Fabris L, Strazzabosco M. Low-Dose Paclitaxel Reduces S100A4 Nuclear Import to Inhibit Invasion and Hematogenous Metastasis of Cholangiocarcinoma. Cancer Research 2016, 76: 4775-4784. PMID: 27328733, PMCID: PMC4987167, DOI: 10.1158/0008-5472.can-16-0188.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAnimalsAntineoplastic Agents, PhytogenicBile Duct NeoplasmsBlotting, WesternCell Line, TumorCell ProliferationCholangiocarcinomaHumansMiceMice, SCIDNeoplasm InvasivenessNeoplasm MetastasisPaclitaxelS100 Calcium-Binding Protein A4SumoylationXenograft Model Antitumor AssaysConceptsLow-dose paclitaxelNuclear S100A4Nuclear expressionSCID mouse xenograft modelPrimary liver cancerLocal tumor growthEGI-1 cellsCandidate therapeutic targetMouse xenograft modelMMP-9 secretionCholangiocarcinoma cell linesCholangiocarcinoma invasivenessLung disseminationMT1-MMP expressionCalcium binding proteinDismal prognosisRate of proliferationMetastatic spreadLiver cancerTumor massPaclitaxel treatmentXenograft modelTherapeutic targetTreatment opportunitiesMetastatic progression
2013
Protein kinase a‐dependent pSer675‐β‐catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis
Spirli C, Locatelli L, Morell CM, Fiorotto R, Morton SD, Cadamuro M, Fabris L, Strazzabosco M. Protein kinase a‐dependent pSer675‐β‐catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis. Hepatology 2013, 58: 1713-1723. PMID: 23744610, PMCID: PMC3800498, DOI: 10.1002/hep.26554.Peer-Reviewed Original ResearchConceptsAutosomal recessive polycystic kidney diseaseCongenital hepatic fibrosisCaroli's diseaseΒ-cateninHepatic fibrosisRac-1 inhibitionIntrahepatic bile ductsRecessive polycystic kidney diseasePotential therapeutic targetPolycystic kidney diseaseStimulation of cAMPRac-1 activityE-cadherin expressionBile ductKidney diseaseLiver pathologyCystic dysplasiaMouse modelTherapeutic targetTranscriptional activityNuclear translocationDiseasePKA blockerCholangiocytesFibrosis