2016
Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells
Forloni M, Gupta R, Nagarajan A, Sun LS, Dong Y, Pirazzoli V, Toki M, Wurtz A, Melnick MA, Kobayashi S, Homer RJ, Rimm DL, Gettinger SJ, Politi K, Dogra SK, Wajapeyee N. Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells. Cell Reports 2016, 16: 457-471. PMID: 27346347, PMCID: PMC4945411, DOI: 10.1016/j.celrep.2016.05.087.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsBrain NeoplasmsCCAAT-Enhancer-Binding ProteinsCell Line, TumorCpG IslandsDNA MethylationDrug Screening Assays, AntitumorErbB ReceptorsGene Expression Regulation, NeoplasticGene SilencingGlioblastomaHumansLung NeoplasmsMAP Kinase Signaling SystemMixed Function OxygenasesMutationOncogenesProtein Kinase InhibitorsProto-Oncogene ProteinsTranscription, GeneticTumor Suppressor ProteinsUp-RegulationConceptsOncogenic epidermal growth factor receptorMethylation-mediated transcriptional silencingEpidermal growth factor receptorTumor suppressorTranscriptional silencingActive DNA demethylationCancer cellsFamily member 1TET1 knockdownDNA demethylaseDNA demethylationTranscription factorsGrowth factor receptorEctopic expressionCytoplasmic localizationGlioblastoma tumor growthLung cancer cellsTET1 expressionFunctional roleSuppressorFactor receptorMember 1TET1SilencingLung cancer samples
2009
Analysis of Drosophila Segmentation Network Identifies a JNK Pathway Factor Overexpressed in Kidney Cancer
Liu J, Ghanim M, Xue L, Brown CD, Iossifov I, Angeletti C, Hua S, Nègre N, Ludwig M, Stricker T, Al-Ahmadie HA, Tretiakova M, Camp RL, Perera-Alberto M, Rimm DL, Xu T, Rzhetsky A, White KP. Analysis of Drosophila Segmentation Network Identifies a JNK Pathway Factor Overexpressed in Kidney Cancer. Science 2009, 323: 1218-1222. PMID: 19164706, PMCID: PMC2756524, DOI: 10.1126/science.1157669.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsApoptosisCarcinoma, Renal CellCell LineCompound Eye, ArthropodDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianFushi Tarazu Transcription FactorsGene Expression ProfilingGene Regulatory NetworksHomeodomain ProteinsHumansJanus KinasesKidneyKidney NeoplasmsMolecular Sequence DataNervous SystemNuclear ProteinsPhosphoprotein PhosphatasesPhosphorylationRepressor ProteinsSignal TransductionTranscription FactorsTranscription, GeneticConceptsTranscription factorsClear cell renal cell carcinomaCell renal cell carcinomaKey transcription factorDrosophila segmentation networkConserved roleEmbryonic segmentationDrosophila melanogasterUbiquitin E3JNK signalingDependent apoptosisSPOPRenal cell carcinomaSPOP expressionKidney cancerTumor necrosis factorNew roleDrosophilaMelanogasterPuckeredGenesSignalingOverexpressedIdentificationApoptosis
1999
Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer.
Caca K, Kolligs FT, Ji X, Hayes M, Qian J, Yahanda A, Rimm DL, Costa J, Fearon ER. Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer. Molecular Cancer Research 1999, 10: 369-76. PMID: 10392898.Peer-Reviewed Original ResearchMeSH KeywordsAdenomatous Polyposis Coli ProteinAmino Acid SequenceAnimalsBeta CateninCadherinsCytoskeletal ProteinsDesmoplakinsDNA-Binding ProteinsGamma CateninGene Expression Regulation, NeoplasticHMGB ProteinsHumansLymphoid Enhancer-Binding Factor 1Molecular Sequence DataMutagenesisPancreatic NeoplasmsStomach NeoplasmsTCF Transcription FactorsTrans-ActivatorsTranscription Factor 7-Like 1 ProteinTranscription FactorsTranscription, GeneticTumor Cells, CulturedConceptsPhosphorylation sitesMutant proteinsGlycogen synthase kinase 3beta phosphorylation sitesGlycogen synthase kinase-3betaFactor transcription factorsPotential phosphorylation sitesSynthase kinase-3betaTCF transcriptional activityE-cadherin inactivationNH2-terminal deletionsRole of APCImportant binding partnerSerine 28TCF transcriptionTranscriptional deregulationT-cell factorBinding partnerTranscription factorsAPC proteinKinase-3betaTranscriptional activityNH2 terminusAdenomatous polyposis coli (APC) mutationsCell adhesionPancreatic cancer linesFrequent Nuclear/Cytoplasmic Localization of β-Catenin without Exon 3 Mutations in Malignant Melanoma
Rimm D, Caca K, Hu G, Harrison F, Fearon E. Frequent Nuclear/Cytoplasmic Localization of β-Catenin without Exon 3 Mutations in Malignant Melanoma. American Journal Of Pathology 1999, 154: 325-329. PMID: 10027390, PMCID: PMC1850000, DOI: 10.1016/s0002-9440(10)65278-9.Peer-Reviewed Original ResearchConceptsCytoplasmic localizationPhosphorylation sitesE-cadherin-mediated cell-cell adhesionGlycogen synthase kinase 3beta phosphorylation sitesMelanoma cell linesN-terminal phosphorylation sitesWnt pathwayExon 3 mutationsCell linesGlycogen synthase kinase-3betaFactor transcription factorsBeta-catenin accumulatesCell-cell adhesionSynthase kinase-3betaBeta-catenin exon 3 mutationsDNA sequencing studiesAdenomatous polyposis coliAxin proteinTranscription factorsKinase-3betaAmino terminusBeta-CateninBeta-catenin mutationsWnt pathway activationSequencing studies