Featured Publications
Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition
Gale M, Li Y, Cao J, Liu ZZ, Holmbeck MA, Zhang M, Lang SM, Wu L, Do Carmo M, Gupta S, Aoshima K, DiGiovanna MP, Stern DF, Rimm DL, Shadel GS, Chen X, Yan Q. Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition. Cancer Research 2020, 80: 524-535. PMID: 31690671, PMCID: PMC7002225, DOI: 10.1158/0008-5472.can-18-3985.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBreast NeoplasmsCell ProliferationDrug Resistance, NeoplasmEnzyme InhibitorsFemaleHumansMiceMice, Inbred NODMice, SCIDMitochondrial Proton-Translocating ATPasesOligomycinsReceptor, ErbB-2TrastuzumabTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsResistant cellsHER2-Targeted TherapyTrastuzumab-resistant tumorsNew therapeutic strategiesNovel potential targetDrug-free mediumAntibody therapySynthase inhibitionLow doseTherapeutic strategiesTrastuzumabBreast tumorsHER2TherapyAcquired ResistanceTumorsPotential targetMitochondrial respirationCellsSelective dependencyInhibitionMinimal changesNovel vulnerabilitiesATP synthase inhibitionOligomycin AKDM5 lysine demethylases are involved in maintenance of 3′UTR length
Blair LP, Liu Z, Labitigan RL, Wu L, Zheng D, Xia Z, Pearson EL, Nazeer FI, Cao J, Lang SM, Rines RJ, Mackintosh SG, Moore CL, Li W, Tian B, Tackett AJ, Yan Q. KDM5 lysine demethylases are involved in maintenance of 3′UTR length. Science Advances 2016, 2: e1501662. PMID: 28138513, PMCID: PMC5262454, DOI: 10.1126/sciadv.1501662.Peer-Reviewed Original ResearchMeSH Keywords3' Untranslated RegionsBreast NeoplasmsCyclin D1DEAD-box RNA HelicasesFemaleHumansJumonji Domain-Containing Histone DemethylasesMCF-7 CellsNeoplasm ProteinsNuclear ProteinsRepressor ProteinsRetinoblastoma-Binding Protein 2Ribonuclease IIISaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsConceptsAlternative mRNA formsLysine demethylasesLysine demethylasePolyadenylation sitesJhd2Novel roleProcessing machineryKDM5B expressionMRNA formsBreast cancer cellsDemethylasesTargetable mechanismHuman breast tumor tissuesKDM5BProtein expressionCancer cellsKDM5AGenesCritical roleBreast tumor tissuesCellsExpressionChromatinSaccharomycesDemethylase
2022
CECR2 drives breast cancer metastasis by promoting NF-κB signaling and macrophage-mediated immune suppression
Zhang M, Liu ZZ, Aoshima K, Cai WL, Sun H, Xu T, Zhang Y, An Y, Chen JF, Chan LH, Aoshima A, Lang SM, Tang Z, Che X, Li Y, Rutter SJ, Bossuyt V, Chen X, Morrow JS, Pusztai L, Rimm DL, Yin M, Yan Q. CECR2 drives breast cancer metastasis by promoting NF-κB signaling and macrophage-mediated immune suppression. Science Translational Medicine 2022, 14: eabf5473. PMID: 35108062, PMCID: PMC9003667, DOI: 10.1126/scitranslmed.abf5473.Peer-Reviewed Original ResearchConceptsBreast cancer metastasisReticuloendotheliosis viral oncogene homolog ACancer metastasisImmune suppressionM2 macrophagesWorse metastasis-free survivalMetastatic breast cancerMetastasis-free survivalV-rel avian reticuloendotheliosis viral oncogene homolog ACancer-related deathPrimary breast tumorsMultiple mouse modelsNF-κB signalingImmunocompetent settingNuclear factor-κB family membersMetastasis-promoting genesDistant metastasisMetastatic sitesPrimary tumorEffective therapyBreast cancerMetastasis treatmentMouse modelBreast tumorsMetastasis