2019
Synergistic inhibition of GP130 and ERK signaling blocks chemoresistant bladder cancer cell growth
Li X, He S, Tian Y, Weiss RM, Martin DT. Synergistic inhibition of GP130 and ERK signaling blocks chemoresistant bladder cancer cell growth. Cellular Signalling 2019, 63: 109381. PMID: 31374291, DOI: 10.1016/j.cellsig.2019.109381.Peer-Reviewed Original ResearchMeSH KeywordsButadienesCarcinoma, Transitional CellCell Line, TumorCell MovementCell SurvivalDrug Resistance, NeoplasmDrug SynergismEnzyme InhibitorsGene Expression Regulation, NeoplasticGlycoproteinsHumansHydrazinesMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1NitrilesQuinoxalinesUrinary Bladder NeoplasmsConceptsChemoresistant bladder cancerBladder cancer cellsBladder cancerInterleukin-6Clinical outcomesMultidrug resistanceGemcitabine-resistant bladder cancer cellsBladder cancer cell growthMajor treatment obstacleMetastatic bladder cancerPI3K/Akt/mTOR signalingCancer cellsResistant bladder cancer cellsPoor clinical outcomeAkt/mTOR SignalingSynergistic inhibitionNovel therapeutic strategiesPotential therapeutic targetMEK/ERK signalingCancer cell growthRaf/MEK/ERK signalingRole of gp130Therapeutic strategiesTreatment obstaclesTherapeutic targetGlycoprotein-130 expression is associated with aggressive bladder cancer and is a potential therapeutic target
Martin DT, Shen H, Steinbach-Rankins JM, Zhu X, Johnson KK, Syed J, Saltzman WM, Weiss RM. Glycoprotein-130 expression is associated with aggressive bladder cancer and is a potential therapeutic target. Molecular Cancer Therapeutics 2019, 18: molcanther.1079.2017. PMID: 30381445, PMCID: PMC6363894, DOI: 10.1158/1535-7163.mct-17-1079.Peer-Reviewed Original ResearchConceptsBladder cancer cell linesBladder tumorsBladder cancerCancer cell linesHigh-grade bladder cancer cell linesCancer xenograft mouse modelBladder cancer growthAggressive bladder cancerPotential therapeutic targetHuman bladder tumorsXenograft mouse modelBladder cancer progressionCell linesBladder tumor cellsCurative potentialOptimal treatmentTumor gradePatient outcomesReduced cell migrationTumor volumeTumor categoryMouse modelTherapeutic targetTumor aggressivenessCancer growth
2013
Nanoparticles for urothelium penetration and delivery of the histone deacetylase inhibitor belinostat for treatment of bladder cancer
Martin DT, Hoimes CJ, Kaimakliotis HZ, Cheng CJ, Zhang K, Liu J, Wheeler MA, Kelly WK, Tew GN, Saltzman WM, Weiss RM. Nanoparticles for urothelium penetration and delivery of the histone deacetylase inhibitor belinostat for treatment of bladder cancer. Nanomedicine Nanotechnology Biology And Medicine 2013, 9: 1124-1134. PMID: 23764660, PMCID: PMC3815967, DOI: 10.1016/j.nano.2013.05.017.Peer-Reviewed Original ResearchConceptsHistone deacetylase inhibitor belinostatBladder cancerBladder permeability barrierNon-invasive bladder cancerCultured bladder cancer cellsBladder cancer cellsChemotherapy efficacyIntravesical drug deliveryXenograft tumorsMouse bladderMouse modelConvincing dataHuman ureterBelinostatCancerCancer cellsLower IC50TumorsAcetyl-H4Tissue penetrationCLINICAL EDITORIntracellular uptakeDeliveryCellsPatients
2006
A role for Akt in the rapid regulation of inflammatory and apoptotic pathways in mouse bladder
Tamarkin FJ, Kang WS, Cohen JJ, Wheeler MA, Weiss RM. A role for Akt in the rapid regulation of inflammatory and apoptotic pathways in mouse bladder. Naunyn-Schmiedeberg's Archives Of Pharmacology 2006, 373: 349-359. PMID: 16832691, DOI: 10.1007/s00210-006-0081-2.Peer-Reviewed Original ResearchConceptsApoptotic pathwayPI3KAkt phosphorylationNon-phosphorylated speciesPhosphatidylinositol-3 kinaseNF-κBPhosphorylation of AktPI3K/AktCellular signalingTranscription factorsForkhead familyPI3K inhibitorsNF-κB phosphorylationKappa BDownstream pathwaysAkt activationInhibitor kappa BPhosphorylationRapid regulationAktProtein amountNuclear factor kappa BK inhibitorsCancer cellsUrothelial cancer cells