2020
STRIPAK directs PP2A activity toward MAP4K4 to promote oncogenic transformation of human cells
Kim J, Berrios C, Kim M, Schade A, Adelmant G, Yeerna H, Damato E, Iniguez A, Florens L, Washburn M, Stegmaier K, Gray N, Tamayo P, Gjoerup O, Marto J, DeCaprio J, Hahn W. STRIPAK directs PP2A activity toward MAP4K4 to promote oncogenic transformation of human cells. ELife 2020, 9: e53003. PMID: 31913126, PMCID: PMC6984821, DOI: 10.7554/elife.53003.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsCalmodulin-Binding ProteinsCell ProliferationCell Transformation, NeoplasticFemaleGene Knockdown TechniquesHEK293 CellsHeterograftsHumansIntracellular Signaling Peptides and ProteinsMicePhosphoprotein PhosphatasesProtein Serine-Threonine KinasesSignal TransductionTranscription FactorsYAP-Signaling ProteinsConceptsStriatin-interacting phosphatase and kinaseSV40 small t antigenB subunitCell transformationPP2A subunitsHippo pathway effector YAP1Regulatory B subunitPP2A B subunitsPP2A-mediated dephosphorylationSmall t antigenInduce cell transformationPP2A functionPP2A complexPP2A activityOncogenic transformationSubunit interactionsPP2AHuman cancersT antigenMAP4K4SubunitAssociated with STCell alterationsPartial lossCells
2018
Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS
Kitajima S, Asahina H, Chen T, Guo S, Quiceno L, Cavanaugh J, Merlino A, Tange S, Terai H, Kim J, Wang X, Zhou S, Xu M, Wang S, Zhu Z, Thai T, Takahashi C, Wang Y, Neve R, Stinson S, Tamayo P, Watanabe H, Kirschmeier P, Wong K, Barbie D. Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS. Cancer Cell 2018, 34: 439-452.e6. PMID: 30205046, PMCID: PMC6422029, DOI: 10.1016/j.ccell.2018.08.009.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsAntineoplastic Agents, ImmunologicalCarcinoma, Non-Small-Cell LungCell Line, TumorDisease Models, AnimalDrug Resistance, NeoplasmHEK293 CellsHumansImmunity, InnateInsulin-Like Growth Factor ILung NeoplasmsMiceMice, TransgenicMitogen-Activated Protein Kinase KinasesPhosphoproteinsProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins p21(ras)Transcription FactorsYAP-Signaling ProteinsConceptsGenetically engineered mouse modelsMediators of acquired resistanceDownstream of KRASBET inhibitor JQ1Effective therapeutic strategyTumor shrinkageTargeted therapyIntermittent treatmentYAP1 signalingMouse modelPathway inhibitionBET inhibitionTherapeutic strategiesInhibitor JQ1YAP1 upregulationOncogenic KRASBET inhibitorsOvercome resistancePromoter acetylationIntrinsic resistancePotential translationKRASMEKInnateInhibition
2014
KRAS and YAP1 Converge to Regulate EMT and Tumor Survival
Shao D, Xue W, Krall E, Bhutkar A, Piccioni F, Wang X, Schinzel A, Sood S, Rosenbluh J, Kim J, Zwang Y, Roberts T, Root D, Jacks T, Hahn W. KRAS and YAP1 Converge to Regulate EMT and Tumor Survival. Cell 2014, 158: 171-184. PMID: 24954536, PMCID: PMC4110062, DOI: 10.1016/j.cell.2014.06.004.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell SurvivalColonic NeoplasmsDrug Delivery SystemsDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHCT116 CellsHumansLung NeoplasmsMicePhosphoproteinsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Ras ProteinsSignal TransductionTranscription FactorsTranscriptional ActivationYAP-Signaling ProteinsConceptsEpithelial-mesenchymal transitionTranscriptional regulator of epithelial-mesenchymal transitionOncogenic Ras signalingColon cancer cell linesTranscriptional coactivator YAP1KRAS-dependent cellsRegulator of epithelial-mesenchymal transitionMurine lung cancer modelTranscriptional regulationCancer cell linesMutant allelesRas signalingTranscription factor FosOncogenic RasTranscriptional programsLung cancer modelRegulating epithelial-mesenchymal transitionMolecular basisOncogenic alleleCell transformationYAP1YAP1 signalingPromote survivalCancer cellsOncogenic dependency