Xiaoling Li, PhD
Associate Research ScientistDownloadHi-Res Photo
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Titles
Associate Research Scientist
Associate Research Scientist, Urology
Departments & Organizations
- Mu Lab
Education & Training
- Postdoc Researcher
- UT Southwestern Medical Center
- PhD
- Zhejiang University, Life Sciences Institute/Cell Biology
Research
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Overview
Public Health Interests
Cancer; Genetics, Genomics, Epigenetics
Research at a Glance
Yale Co-Authors
Frequent collaborators of Xiaoling Li's published research.
Ping Mu, PhD
Su Deng, PhD
Publications
Featured Publications
Loss of SYNCRIP unleashes APOBEC-driven mutagenesis, tumor heterogeneity, and AR-targeted therapy resistance in prostate cancer
Li X, Wang Y, Deng S, Zhu G, Wang C, Johnson N, Zhang Z, Tirado C, Xu Y, Metang L, Gonzalez J, Mukherji A, Ye J, Yang Y, Peng W, Tang Y, Hofstad M, Xie Z, Yoon H, Chen L, Liu X, Chen S, Zhu H, Strand D, Liang H, Raj G, He H, Mendell J, Li B, Wang T, Mu P. Loss of SYNCRIP unleashes APOBEC-driven mutagenesis, tumor heterogeneity, and AR-targeted therapy resistance in prostate cancer. Cancer Cell 2023, 41: 1427-1449.e12. PMID: 37478850, PMCID: PMC10530398, DOI: 10.1016/j.ccell.2023.06.010.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsProstate cancerTherapy resistanceTumor heterogeneityTumor mutational burdenCell-intrinsic mechanismsPromote tumor heterogeneityMutational burdenTargeted therapyDriver mutationsPCa cellsCancer cellsHuman cancersMutated genesCancerMutational signaturesProstateTumorTherapyFOXA1APOBEC proteinsAPOBEC3BEP300Molecular brakeMutationsSYNCRIPLoss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation
Zhang Z, Zhou C, Li X, Barnes S, Deng S, Hoover E, Chen C, Lee Y, Zhang Y, Wang C, Metang L, Wu C, Tirado C, Johnson N, Wongvipat J, Navrazhina K, Cao Z, Choi D, Huang C, Linton E, Chen X, Liang Y, Mason C, de Stanchina E, Abida W, Lujambio A, Li S, Lowe S, Mendell J, Malladi V, Sawyers C, Mu P. Loss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation. Cancer Cell 2020, 37: 584-598.e11. PMID: 32220301, PMCID: PMC7292228, DOI: 10.1016/j.ccell.2020.03.001.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAndrogen AntagonistsAnimalsApoptosisBiomarkers, TumorCell ProliferationChromatinDNA HelicasesDNA-Binding ProteinsDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHigh-Throughput Screening AssaysHumansMaleMiceProstatic Neoplasms, Castration-ResistantReceptors, AndrogenRNA, Small InterferingTranscription FactorsTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsAntiandrogen resistanceChromatin dysregulationCHD1 lossProstate cancerGenomic copy number alterationsRNA-seq analysisResistance to hormonal therapyCopy number alterationsAR-targeted therapiesMetastatic prostate cancerATAC-seqClosed chromatinRNA-seqTranscriptional plasticityTranscription factorsFunctional screeningTranscriptomic changesMechanisms of resistanceHormone therapyLineage programsChromatinCHD1Global changeIntegrated analysisTherapy
2025
Lineage plasticity and histological transformation: tumor histology as a spectrum
Li X, Gardner E, Molina-Pinelo S, Wilhelm C, Mu P, Quintanal-Villalonga Á. Lineage plasticity and histological transformation: tumor histology as a spectrum. Cell Research 2025, 35: 803-823. PMID: 41023204, PMCID: PMC12589604, DOI: 10.1038/s41422-025-01180-x.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHistological transformationLineage plasticityIn vivo modelsPatients treated with targeted therapyHigh risk of transformationResistance to anticancer therapiesMechanisms of tumor evolutionClinical settingRisk of transformationHuman tumor samplesAnalysis of human tumor samplesTumor histologyProstatic adenocarcinomaNeuroendocrine transformationTherapeutic overviewBiomarkers PredictiveTumor samplesLung adenocarcinomaAnticancer therapyMolecular findingsTumor evolutionMolecular driversTumorSquamous transdifferentiationTherapy
2024
Restoring our ubiquitination machinery to overcome resistance in cancer therapy
Li X, Mu P. Restoring our ubiquitination machinery to overcome resistance in cancer therapy. Oncoscience 2024, 11: 43-44. PMID: 38711948, PMCID: PMC11073315, DOI: 10.18632/oncoscience.600.Commentaries, Editorials and LettersCitationsAltmetricZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer
Xu Y, Yang Y, Wang Z, Sjostrom M, Jiang Y, Tang Y, Cheng S, Deng S, Wang C, Gonzalez J, Johnson N, Li X, Li X, Metang L, Mukherji A, Xu Q, Tirado C, Wainwright G, Yu X, Barnes S, Hofstad M, Chen Y, Zhu H, Hanker A, Raj G, Zhu G, He H, Wang Z, Arteaga C, Liang H, Feng F, Wang Y, Wang T, Mu P. ZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer. Cancer Discovery 2024, 14: 1496-1521. PMID: 38591846, PMCID: PMC11285331, DOI: 10.1158/2159-8290.cd-23-0539.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLineage plasticityTherapy resistanceProstate cancerCancer cellsAndrogen receptorResistance to AR-targeted therapiesLuminal lineageAR-targeted therapiesOvercome therapy resistanceTransition of cancer cellsEpigenetic regulatory machineryBona fide coactivatorTherapy responseAR signalingEpigenetic rewiringDrug resistanceTherapeutic strategiesEpigenetic reprogrammingProstateTherapyCancerPhenotypic plasticityRegulatory machineryAndrogenTranscriptional programsAbstract 4311: The interplay of SYNCRIP deficiency, APOBEC activity, and extrachromosomal DNA in castration-resistant prostate cancer drug resistance
Li X, Deng S, Wang C, Wang Y, Mu P. Abstract 4311: The interplay of SYNCRIP deficiency, APOBEC activity, and extrachromosomal DNA in castration-resistant prostate cancer drug resistance. Cancer Research 2024, 84: 4311-4311. DOI: 10.1158/1538-7445.am2024-4311.Peer-Reviewed Original ResearchConceptsProstate cancer drug resistanceCancer drug resistanceDrug resistanceProstate cancerTherapy resistanceAmerican Association for Cancer Research annual meetingsResistance to androgen receptor (AR)-targeted therapiesAndrogen receptor (AR)-targeted therapiesIncreased therapy resistanceTumor mutational burdenCRPC cell linesAPOBEC activityCastration-resistant formComplexity of drug resistanceWhole-exome sequencingContribution to drug resistanceDrivers of resistanceIn vivo modelsPatient-derived samplesExtrachromosomal DNAAPOBEC-mediated mutagenesisMutational burdenDNA damageFunctional CRISPR screensTumor behavior
2023
UBE2J1 is the E2 ubiquitin-conjugating enzyme regulating androgen receptor degradation and antiandrogen resistance
Rodriguez Tirado C, Wang C, Li X, Deng S, Gonzalez J, Johnson N, Xu Y, Metang L, Sundar Rajan M, Yang Y, Yin Y, Hofstad M, Raj G, Zhang S, Lemoff A, He W, Fan J, Wang Y, Wang T, Mu P. UBE2J1 is the E2 ubiquitin-conjugating enzyme regulating androgen receptor degradation and antiandrogen resistance. Oncogene 2023, 43: 265-280. PMID: 38030789, PMCID: PMC10798893, DOI: 10.1038/s41388-023-02890-5.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAberrant androgen receptorProstate cancerAR ubiquitinationAR degradationAntiandrogen therapyResistance to antiandrogen therapyE2 ubiquitin-conjugating enzymeEnhanced AR signalingAndrogen receptor degradersAR protein levelsProstate cancer patientsUbiquitin-conjugating enzymeResistant tumorsPCa tumorsAR signalingAndrogen receptorAntiandrogen treatmentAntiandrogen resistanceAR proteinReceptor degradationProtein levelsOncogenic proteinsTumorTherapyProtein degradation processThe Critical Interplay of CAF Plasticity and Resistance in Prostate Cancer.
Li X, Mu P. The Critical Interplay of CAF Plasticity and Resistance in Prostate Cancer. Cancer Research 2023, 83: 2990-2992. PMID: 37504898, DOI: 10.1158/0008-5472.can-23-2260.Commentaries, Editorials and LettersCitationsAltmetricMeSH Keywords and ConceptsConceptsCastration-resistant prostate cancerAndrogen deprivation therapyProstate cancerAndrogen receptorCastration-resistant prostate cancer developmentDevelopment of castration-resistant prostate cancerGenetically engineered mouse modelsMyofibroblastic cancer-associated fibroblastsOvercome treatment resistanceCancer-associated fibroblastsIncreased tumor heterogeneityDeprivation therapyCRPC developmentProstate tumorsTumor microenvironmentLineage plasticityTreatment resistanceStromal compartmentStandard treatmentTumor heterogeneityCancer recurrenceDrug resistanceDisease progressionMouse modelSingle-cell RNA sequencingAbstract PR001: An endogenous molecular brake preventing APOBEC-driven tumor mutational burden, heterogeneity and AR therapy resistance
Mu P, Li X, Wang Y. Abstract PR001: An endogenous molecular brake preventing APOBEC-driven tumor mutational burden, heterogeneity and AR therapy resistance. Cancer Research 2023, 83: pr001-pr001. DOI: 10.1158/1538-7445.prca2023-pr001.Peer-Reviewed Original ResearchConceptsTumor mutational burdenTherapy resistanceMutational burdenMolecular brakeSingle cell RNA-seqDriver mutationsDrivers of mutagenesisClinical outcomes of patientsCRISPR library screensRNA-seqExome-sequencingScRNA-seqOutcomes of patientsLibrary screeningProstate cancer researchFunctional screeningNon-malignant cellsCell-intrinsic mechanismsPromote heterogeneityMutagenesisMutated genesAPOBEC proteinsMutational signaturesPotential therapeutic targetMutationsAbstract 93: An endogenous molecular brake preventing APOBEC-driven tumor mutational burden, heterogeneity and therapy resistance
Mu P, Li X, Wang Y, Wang T, Deng S. Abstract 93: An endogenous molecular brake preventing APOBEC-driven tumor mutational burden, heterogeneity and therapy resistance. Cancer Research 2023, 83: 93-93. DOI: 10.1158/1538-7445.am2023-93.Peer-Reviewed Original ResearchConceptsTumor mutational burdenTherapy resistanceMutational burdenMolecular brakeSingle cell RNA-seqDriver mutationsDrivers of mutagenesisAmerican Association for Cancer Research annual meetingsClinical outcomes of patientsCRISPR library screensRNA-seqExome-sequencingScRNA-seqOutcomes of patientsLibrary screeningFunctional screeningNon-malignant cellsCell-intrinsic mechanismsPromote heterogeneityMutagenesisMutated genesAPOBEC proteinsMutational signaturesMutationsPotential therapeutic target
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