Yao Li, MD
Postdoctoral AssociateAbout
Research
Publications
2024
Combined BET and MEK Inhibition synergistically suppresses melanoma by targeting YAP1
Hu R, Hou H, Li Y, Zhang M, Li X, Chen Y, Guo Y, Sun H, Zhao S, Liao M, Cao D, Yan Q, Chen X, Yin M. Combined BET and MEK Inhibition synergistically suppresses melanoma by targeting YAP1. Theranostics 2024, 14: 593-607. PMID: 38169595, PMCID: PMC10758063, DOI: 10.7150/thno.85437.Peer-Reviewed Original ResearchConceptsMEK inhibitor resistanceMEK inhibitor trametinibTrametinib treatmentInhibitor resistanceInhibitor trametinibMelanoma patientsYAP1 expressionMEK inhibitionBRAF-mutant melanoma patientsResistance to MEK inhibitionYAP1 inhibitionResistance to trametinibMelanoma growth <i>inInhibition of BRD4Trametinib resistanceAntitumor effectMelanoma growthTrametinibNHWD-870YAP1 inhibitorDrug resistanceMelanomaMelanoma samplesMelanoma cellsBRD4 depletion
2023
Design of Class I/IV Bromodomain-Targeting Degraders for Chromatin Remodeling Complexes
Zahid H, Costello J, Li Y, Kimbrough J, Actis M, Rankovic Z, Yan Q, Pomerantz W. Design of Class I/IV Bromodomain-Targeting Degraders for Chromatin Remodeling Complexes. ACS Chemical Biology 2023, 18: 1278-1293. PMID: 37260298, PMCID: PMC10698694, DOI: 10.1021/acschembio.2c00902.Peer-Reviewed Original ResearchConceptsChromatin Remodeling ComplexNon-BET bromodomainsRemodeling complexProtein degradationHeterobifunctional moleculesBET familyProtein targetsPyrimidine base analogsNumber of degradersDegradersOncogenic roleTernary complexExit vectorsWestern blottingProteinFirst exampleClass IChallenging targetComplexesCECR2ChromatinBromodomainsBPTFFamilyNanoBRET
2022
BRD4 inhibitor suppresses melanoma metastasis via the SPINK6/EGFR-EphA2 pathway
Hu R, Li Y, Guo Y, Li X, Du S, Liao M, Hou H, Sun H, Zhao S, Su J, Chen X, Yin M. BRD4 inhibitor suppresses melanoma metastasis via the SPINK6/EGFR-EphA2 pathway. Pharmacological Research 2022, 187: 106609. PMID: 36516883, DOI: 10.1016/j.phrs.2022.106609.Peer-Reviewed Original ResearchCECR2 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
2020
A novel predictive model incorporating immune-related gene signatures for overall survival in melanoma patients
Liao M, Zeng F, Li Y, Gao Q, Yin M, Deng G, Chen X. A novel predictive model incorporating immune-related gene signatures for overall survival in melanoma patients. Scientific Reports 2020, 10: 12462. PMID: 32719391, PMCID: PMC7385638, DOI: 10.1038/s41598-020-69330-2.Peer-Reviewed Original ResearchConceptsImmune-related genesMelanoma patientsGene Expression Omnibus databaseImmune-related gene signatureConventional staging systemsLow-risk patientsIndependent prognostic factorDecision curve analysisCancer Genome Atlas (TCGA) databaseTwo-gene signatureSignature gene expressionIRG signatureOverall survivalPrognostic factorsClinical parametersPrediction nomogramStaging systemTNM stagePatient prognosisConcordance indexPrognostic performanceIndividual prognosisInvasive typeSkin cancerImmune systemPotent BRD4 inhibitor suppresses cancer cell-macrophage interaction
Yin M, Guo Y, Hu R, Cai WL, Li Y, Pei S, Sun H, Peng C, Li J, Ye R, Yang Q, Wang N, Tao Y, Chen X, Yan Q. Potent BRD4 inhibitor suppresses cancer cell-macrophage interaction. Nature Communications 2020, 11: 1833. PMID: 32286255, PMCID: PMC7156724, DOI: 10.1038/s41467-020-15290-0.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAnimalsCell CommunicationCell Cycle ProteinsCell Line, TumorCell ProliferationDisease Models, AnimalDown-RegulationDrug DesignFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMacrophage Colony-Stimulating FactorMacrophagesMice, Inbred BALB CMice, NudeNeoplasmsPhosphorylationProto-Oncogene Proteins c-mycReceptors, Granulocyte-Macrophage Colony-Stimulating FactorSignal TransductionTranscription FactorsTreatment OutcomeConceptsTumor growthMajor clinical stagesBET inhibitorsProliferation of tumorsExtraterminal domain (BET) family proteinsTumor cell proliferationClinical stageTumor shrinkageSyngeneic modelPotent BRD4 inhibitorsSmall molecule inhibitorsSolid tumorsBRD4 inhibitionTumor cellsOral bioavailabilityCancer treatmentCell proliferationBRD4 inhibitorsMolecule inhibitorsMultiple mechanismsC-MycTumorsInhibitorsAcquired 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 A