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
2016
Characterizing genomic alterations in cancer by complementary functional associations
Kim J, Botvinnik O, Abudayyeh O, Birger C, Rosenbluh J, Shrestha Y, Abazeed M, Hammerman P, DiCara D, Konieczkowski D, Johannessen C, Liberzon A, Alizad-Rahvar A, Alexe G, Aguirre A, Ghandi M, Greulich H, Vazquez F, Weir B, Van Allen E, Tsherniak A, Shao D, Zack T, Noble M, Getz G, Beroukhim R, Garraway L, Ardakani M, Romualdi C, Sales G, Barbie D, Boehm J, Hahn W, Mesirov J, Tamayo P. Characterizing genomic alterations in cancer by complementary functional associations. Nature Biotechnology 2016, 34: 539-546. PMID: 27088724, PMCID: PMC4868596, DOI: 10.1038/nbt.3527.Peer-Reviewed Original Research
2015
A Functional Landscape of Resistance to ALK Inhibition in Lung Cancer
Wilson FH, Johannessen CM, Piccioni F, Tamayo P, Kim JW, Van Allen EM, Corsello SM, Capelletti M, Calles A, Butaney M, Sharifnia T, Gabriel SB, Mesirov JP, Hahn WC, Engelman JA, Meyerson M, Root DE, Jänne PA, Garraway LA. A Functional Landscape of Resistance to ALK Inhibition in Lung Cancer. Cancer Cell 2015, 27: 397-408. PMID: 25759024, PMCID: PMC4398996, DOI: 10.1016/j.ccell.2015.02.005.Peer-Reviewed Original ResearchConceptsFunctional genetic studiesG protein-coupled receptorsResistance driversALK inhibitionFunctional landscapeGenetic studiesLung cancer cellsALK inhibitor resistanceResistance pathwaysMechanisms of resistanceReceptor familyPKC activationPurinergic receptor familyPKC inhibitionCrizotinib-resistant ALKCancer cellsInhibitor resistanceGene signatureDependent mechanismLung cancerLung tumorsALK inhibitorsInhibitionALKMechanism
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
2010
An ATM/Chk2-Mediated DNA Damage-Responsive Signaling Pathway Suppresses Epstein-Barr Virus Transformation of Primary Human B Cells
Nikitin P, Yan C, Forte E, Bocedi A, Tourigny J, White R, Allday M, Patel A, Dave S, Kim W, Hu K, Guo J, Tainter D, Rusyn E, Luftig M. An ATM/Chk2-Mediated DNA Damage-Responsive Signaling Pathway Suppresses Epstein-Barr Virus Transformation of Primary Human B Cells. Cell Host & Microbe 2010, 8: 510-522. PMID: 21147465, PMCID: PMC3049316, DOI: 10.1016/j.chom.2010.11.004.Peer-Reviewed Original ResearchMeSH KeywordsAtaxia Telangiectasia Mutated ProteinsB-LymphocytesCell Cycle ProteinsCell ProliferationCell Transformation, ViralCells, CulturedCheckpoint Kinase 2DNA DamageDNA-Binding ProteinsEpstein-Barr Virus Nuclear AntigensHerpesvirus 4, HumanHumansProtein Serine-Threonine KinasesSignal TransductionTumor Suppressor ProteinsConceptsDNA damage responseEpstein-Barr virusPrimary human B cellsHuman B cellsB cellsTumor suppressor mechanismSuppressor mechanismViral latency productsProliferating lymphoblastoid cell linesPrimary B cellsInduce cell immortalizationLymphoblastoid cell linesDDR kinase ATMEarly cell divisionsDNA damage response activationLytic viral replicationIncreased transformation efficiencyLatent episomeKinase ATMImmortalization efficiencyCell divisionHuman malignanciesDamage responseCell immortalizationViral replication