Ping Mu
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Professional Highlights
About
Research
Professional Highlights
About
Research
Professional Highlights
Honors
- 10 National Awards
- 4 Regional Awards
- 1 International Award
Education
PhD
Weill Medical College of Cornell University , Biomedical Sciences (2013)
Weill Medical College of Cornell University , Biomedical Sciences (2013)
BS
Peking University , Biotechnology (2007)
Peking University , Biotechnology (2007)
Training
Postdoctoral Research Associate
Memorial Sloan Kettering Cancer Center (2018)
Memorial Sloan Kettering Cancer Center (2018)
Publications Overview
- 22 Publications
- 3,332 Citations
- 1 Yale Co-Author
Featured Publication
ZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer
Honors
- 10 National Awards
- 4 Regional Awards
- 1 International Award
Education
PhD
Weill Medical College of Cornell University , Biomedical Sciences (2013)
Weill Medical College of Cornell University , Biomedical Sciences (2013)
BS
Peking University , Biotechnology (2007)
Peking University , Biotechnology (2007)
Training
Postdoctoral Research Associate
Memorial Sloan Kettering Cancer Center (2018)
Memorial Sloan Kettering Cancer Center (2018)
Publications Overview
- 22 Publications
- 3,332 Citations
- 1 Yale Co-Author
Featured Publication
ZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer
Honors
- 10 National Awards
- 4 Regional Awards
- 1 International Award
About
Biography
Ping earned his Ph.D. in Biomedical Sciences from Weill Medical College of Cornell University, followed by postdoctoral training under Dr. Charles L. Sawyers at Memorial Sloan Kettering Cancer Center. In mid-2018, he established his own independent laboratory at UT Southwestern as an assistant professor in the Department of Molecular Biology. His remarkable contributions to the cancer research field led to his rapid promotion to tenured associate professor before moving his lab to Yale.
Throughout his career, Ping has been the recipient of numerous prestigious awards and grants, including three NIH R01 Awards (one of which was an R37 MERIT Award), the NIH K99/R00 Pathway to Independence Award, a DoD Idea Development Award, a DoD Idea Expansion Award, two CPRIT awards, as well as distinguished honors like the AACR NextGen Star Award, the Prostate Cancer Foundation Young Investigator Award, the Welch Foundation Research Award, the SBUR Young Investigator Award, and the SAU Rising Star Award. His research, which pushes the boundaries of cancer biology, has been featured in top-tier journals such as Science (2017), Cancer Cell (2020, 2023), Cancer Discovery (2024), Nature Cancer (2022), Nature Genetics (2015), and Oncogene (2024).
When not immersed in science, Ping channels his creativity into a wide range of hobbies—from 3D printing, soccer, and photography to officiating weddings and mastering handyman tasks. He even dabbles in stand-up comedy and pest control. Above all, he cherishes spending time with his son, who dreams of a career of testing waterslides professionally, and his two mischievous corgis, who have a knack for chewing through anything in their path.
Appointments
Departments & Organizations
Education & Training
- Postdoctoral Research Associate
- Memorial Sloan Kettering Cancer Center (2018)
- PhD
- Weill Medical College of Cornell University , Biomedical Sciences (2013)
- BS
- Peking University , Biotechnology (2007)
Research
Overview
Our lab is dedicated to uncovering the molecular mechanisms that drive resistance to targeted and immune therapies in prostate and other cancers. We are also pioneering innovative therapeutic strategies to overcome these resistances, utilizing a range of state-of-the-art techniques, including 3D-cultured organoids, single-cell sequencing, and spatial transcriptomics. Our recent work has been published in top-tier journals such as Cancer Cell (2020, 2023), Cancer Discovery (2024), Nature Cancer (2022), and Oncogene (2024).
Exciting Research Directions in the Lab:
- Lineage Plasticity and Resistance: Unravel the mechanisms of lineage plasticity-driven resistance and develop novel combination therapies to prevent or overcome this resistance.
- Novel Tumor Suppressors and Oncogenes: Identify and explore new druggable targets among novel tumor suppressors and oncogenes that mediate therapy resistance.
- Tumor Microenvironment and Immune Modulation: Explore how prostate cancer cells alter the tumor microenvironment and immune cells to achieve resistance.
- Mutagenesis and Tumor Evolution: Investigate the molecular mechanisms that promote mutagenesis, tumor heterogeneity, and tumor evolution.
- Epigenetic Rewiring: Examine how epigenetic rewiring promotes therapy resistance and find ways to counteract these changes.
- Drug development: Develop novel therapeutic agents, including small molecular inhibitors and protein degraders, using our established high-throughput platform.
Medical Subject Headings (MeSH)
Prostate
ORCID
0000-0003-0955-0896
Research at a Glance
Publications Timeline
A big-picture view of Ping Mu's research output by year.
Yale Co-Authors
Frequent collaborators of Ping Mu's published research.
22Publications
3,332Citations
Publications
Featured Publications
ZNF397 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 programsUBE2J1 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 processLoss 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 brakeMutationsSYNCRIPEctopic JAK–STAT activation enables the transition to a stem-like and multilineage state conferring AR-targeted therapy resistance
Deng S, Wang C, Wang Y, Xu Y, Li X, Johnson N, Mukherji A, Lo U, Xu L, Gonzalez J, Metang L, Ye J, Tirado C, Rodarte K, Zhou Y, Xie Z, Arana C, Annamalai V, Liu X, Vander Griend D, Strand D, Hsieh J, Li B, Raj G, Wang T, Mu P. Ectopic JAK–STAT activation enables the transition to a stem-like and multilineage state conferring AR-targeted therapy resistance. Nature Cancer 2022, 3: 1071-1087. PMID: 36065066, PMCID: PMC9499870, DOI: 10.1038/s43018-022-00431-9.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsJAK-STAT activationJanus kinase (JAK)-signal transducerTherapy resistanceLineage plasticityTranscriptional programsJAK-STATAR-targeted therapiesLineage programsLineagesMolecular mechanismsTranscriptomic aberrationsPharmaceutical inhibitionProstate cancerTargeted therapyStem-likeTherapeutic targetTherapyLoss 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 analysisTherapySOX2 promotes lineage plasticity and antiandrogen resistance in TP53- and RB1-deficient prostate cancer
Mu P, Zhang Z, Benelli M, Karthaus W, Hoover E, Chen C, Wongvipat J, Ku S, Gao D, Cao Z, Shah N, Adams E, Abida W, Watson P, Prandi D, Huang C, de Stanchina E, Lowe S, Ellis L, Beltran H, Rubin M, Goodrich D, Demichelis F, Sawyers C. SOX2 promotes lineage plasticity and antiandrogen resistance in TP53- and RB1-deficient prostate cancer. Science 2017, 355: 84-88. PMID: 28059768, PMCID: PMC5247742, DOI: 10.1126/science.aah4307.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLineage plasticityRB1 functionHuman prostate cancer modelProstate cancer modelLoss of TP53Basal-like cellsTumor suppressor geneTranscription factor Sox2Antiandrogen therapyProstate cancerInhibiting Sox2 expressionLineage switchAntiandrogen resistanceCancer modelsTumor cellsSuppressor geneSOX2 expressionIncreased expressionTP53TumorCell lineagesCellular plasticityIn vitroPhenotypic shiftCancerAn allelic series of miR-17∼92–mutant mice uncovers functional specialization and cooperation among members of a microRNA polycistron
Han Y, Vidigal J, Mu P, Yao E, Singh I, González A, Concepcion C, Bonetti C, Ogrodowski P, Carver B, Selleri L, Betel D, Leslie C, Ventura A. An allelic series of miR-17∼92–mutant mice uncovers functional specialization and cooperation among members of a microRNA polycistron. Nature Genetics 2015, 47: 766-775. PMID: 26029871, PMCID: PMC4485521, DOI: 10.1038/ng.3321.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsApoptosisB-LymphocytesCarcinogenesisCells, CulturedEyelidsGene FrequencyGenes, LethalGenome-Wide Association StudyIntellectual DisabilityLimb Deformities, CongenitalMaleMice, 129 StrainMice, Inbred C57BLMice, TransgenicMicrocephalyMicroRNAsMultigene FamilyMutationTracheoesophageal Fistula
2024
Mapping cellular interactions from spatially resolved transcriptomics data
Zhu J, Wang Y, Chang W, Malewska A, Napolitano F, Gahan J, Unni N, Zhao M, Yuan R, Wu F, Yue L, Guo L, Zhao Z, Chen D, Hannan R, Zhang S, Xiao G, Mu P, Hanker A, Strand D, Arteaga C, Desai N, Wang X, Xie Y, Wang T. Mapping cellular interactions from spatially resolved transcriptomics data. Nature Methods 2024, 1-13. PMID: 39227721, DOI: 10.1038/s41592-024-02408-1.Peer-Reviewed Original ResearchAltmetricHyd/UBR5 defines a tumor suppressor pathway that links Polycomb repressive complex to regulated protein degradation in tissue growth control and tumorigenesis
Wen P, Lei H, Deng H, Deng S, Tirado C, Wang M, Mu P, Zheng Y, Pan D. Hyd/UBR5 defines a tumor suppressor pathway that links Polycomb repressive complex to regulated protein degradation in tissue growth control and tumorigenesis. Genes & Development 2024, 38: 675-691. PMID: 39137945, PMCID: PMC11368183, DOI: 10.1101/gad.351856.124.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsPolycomb Repressive Complex1Tumor suppressor pathwayTissue growth controlSuppressor pathwayProtein degradationZinc finger genesGrowth controlUbiquitin-mediated degradationE3 ubiquitin ligasePolycomb repressive complexesProtein degradation pathwaysTumor suppressor geneHyperplastic discsFinger genesMammalian homologSubstrate adaptorRepressive complexesUbiquitin ligaseEmbryonic segmentationProtein complexesModel organismsHuman geneticsUpstream regulatorSuppressor geneProstate cancer tumorigenesisRestoring 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.Peer-Reviewed Original ResearchAltmetric
Academic Achievements & Community Involvement
honor R01 Research Award
National AwardNIHDetails07/15/2024United Stateshonor R01 Research Award
National AwardNIHDetails05/15/2024United Stateshonor CPRIT Research Award
Regional AwardCancer Prevention and Research Institute of TexasDetails03/01/2022United Stateshonor Idea Expansion Award
National AwardDepartment of DefenseDetails09/01/2021United Stateshonor R37 MERIT Award
National AwardNIHDetails05/15/2021United States
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