Yibin Deng, MD, PhD


Yibin Deng

Contact Info


Office Address:
3-135, Cancer and Cardiovascular Research Building,
2231, 6th. St. SE, Minneapolis, MN, 55455

Lab Address:
3-230, Cancer and Cardiovascular Research Building,
2231, 6th. St. SE, Minneapolis, MN, 55455



Dr. Yibin Deng received his M.D. from North Sichuan Medical College and Ph.D. in Pathology from Jilin University Norman Bethune Medical Health Science Center, China. He did his postdoctoral training at New York University and Baylor College of Medicine. In 2005, he joined the Department of Genetics as an Assistant Professor at the University of Texas M.D. Anderson Cancer Center. Dr. Deng was recruited to The Hormel Institute, University of Minnesota as an Assistant Professor in 2009 to lead the Section of Cell Death and Cancer Genetics. In 2019, he was promoted as an I.J. Holton Professor in the Hormel Institute. In 2020, Dr. Deng relocated to The University of Minnesota Medical School as a Professor in the Department of Urology. He is a current member of Masonic Cancer Center and a graduate faculty of M.S. and Ph.D. Programs in Bioinformatics and Computational Biology (BICB) at the University of Minnesota.


Generation and establishment of experimental models that recapitulate the salient features of human cancers harboring various types of genetic changes (prostate, breast, lung, and colon) for oncology research and cancer medicine utilizing human organoids, patient-derived xenograft (PDX) models, and genetically engineered mouse models (GEMMs); Cancer Genetics; Cancer Cell Death (Apoptosis, Necroptosis, Ferroptosis, Pyroptosis and Autophagic Cell Death); Cell/Tissue Metabolomics; Structural Biology (X-Ray crystallography and Cryo-electron microscopy) and Computational Bioinformatics. 

Awards & Recognition

Standing Member, National Cancer Institute-K Series Grant 2019-2023

Howard Temin Award, National Cancer Institute 2007-2013

Scholar Awards of 93rd American Association for Cancer Research (AACR) Annual Meeting 2002


Research Summary/Interests

Deng laboratory focuses on addressing two fundamental questions of cancer biology: how normal cells become cancer cells, and how to selectively kill cancer cells. The Deng lab has been developing four major areas to study prostate cancer by employing a combination of multiple approaches, including conditional gene knock-out/knock-in, genome editing (CRISPR-Cas9), X-ray crystallography/Cryo-EM, and structure-based virtual screening combined with drug design and chemical synthesis.

(1) Discovery of metabolic targets for currently incurable castration-resistant prostate cancer (CRPC)

Through genetic and pharmacological studies, Deng laboratory demonstrated for the first time that hexokinase 2 (HK2)-mediated Warburg effect plays an important role in tumor growth of CRPC in vivo. Dr. Deng has been building a strong cross-functional collaboration team comprising medicinal chemists, structural and computational biologists to dissect the function of HK2-translation axis in prostate tumorigenesis and discover HK2-selective inhibitors to block HK2-driven tumor growth. Utilizing genetic screening and cell metabolomics, they have identified a crucial molecular target that switches Warburg effect into the mitochondrial-dependent oxidative phosphorylation (OXPHOS) signaling, which in turn is essential for prostate cancer cell survival and tumor development under tumor microenvironment. Various types of experimental models are being used to determine the function of cancer metabolic networks in prostate tumor initiation, progression and metastasis.

(2) Structural and functional understanding of oncogene mRNA translation in prostate tumorigenesis

Phosphatase and tensin homolog (PTEN) is a tumor suppressor gene that plays a key role in controlling oncogene mRNA translation through the human translation initiation eIF4E/eIF4G/eIF4A(eIF4F) complex. The Deng lab is interested in deciphering how the eukaryotic eIF4F complex regulates oncogene mRNA translation in prostate tumorigenesis using structural biology methods (X-ray crystallography and Cryo-electron microscopy) coupled with biological studies. The results from these studies will facilitate a structure-based discovery of small-molecule compounds disrupting the assembly of a functional eIF4F complex in prostate cancer cells to selectively block the PTEN loss-driven oncogenic protein synthesis axis and thus inhibit prostate tumor development in vivo.

(3) Dissect the role of dysfunctional telomere-initiated immune response in prostate tumorigenesis

Telomeres are nucleoprotein complex structures that protect chromosomal ends from being recognized as aberrant damaged DNA. Dysfunctional telomeres could arise either from progressive telomere attrition (telomere shortening) or when components of the telomeric DNA-binding proteins (“shelterin complex”) are perturbed (telomere uncapping). The Deng lab has generated a novel in vivo prostate cancer mouse model to study the role of uncapped telomeres in tumorigenesis. Utilizing the genetically engineered mouse models, they have revealed that a dysfunctional telomere-initiated DNA damage response induces an intrinsic cell death signaling in cancer cells with a concurrent activation of innate immune checkpoints extrinsically to remarkably diminish prostate cancer cells. These unexpected studies could provide an effective targeting therapeutic strategy through telomere uncapping-initiated immune response to selectively erase prostate cancer cells.

(4) Gain-of-function of mutant p53 in PTEN loss-driven prostate tumorigenesis

The recent comprehensive sequencing studies revealed that the TP53 gene encoding a tumor suppressor protein is mutated in over 40% of metastatic human prostate cancer. Alterations of TP53 in cancer cells occur predominantly through missense mutations, including six “hotspot” mutations carrying most frequently substitutes, which ultimately result in accumulation of a full-length mutant p53 protein.These mutant p53 proteins not only lead to loss of tumor suppressive function of wild-type p53, but also confer “gain-of-function” (GOF) oncogenic activities that enhance tumor progression and metastasis. Interestingly, the TP53 mutation and loss of PTEN co-exist in metastatic prostate cancer. Owing to technical challenges, a mouse model harboring loss of Pten but expression of a mutant p53 does not exist. To circumvent these deficiencies, the Deng lab has been developing prostate cancer mouse models using a combination of a Pten conditional knockout mouse, p53 conditional knock out and a mutant p53 “hot spot” (identified in prostate cancer patients) knock-in mouse model, in which expression of mutant p53 could be conditionally induced while the expression of wild type p53 and/or Pten could be conditionally deleted in a prostate tissue-specific manner. These mouse models would provide a therapeutic model for drug discovery in vivo and faithfully recapitulate the crucial roles that PTEN loss and mutant p53 expression play during prostate tumor initiation, progression, and metastasis in situ


  • Shi W, Jiang Y, Deng Y, Dong Z, Liu B. Visualization of two architectures in class-II CAP-dependent transcription activation. PLoS Biol 2020;18(4): e3000706.
  • Li Y, Liu Y, Xu H, Jiang G, Van der Jeught K, Fang Y, Zhou Z, Zhang L, Frieden M, Wang L, Luo Z, Radovich M, Schneider BP, Deng Y, Liu Y, Huang K, He B, Wang J, He X, Zhang X, Ji G, Lu X. Heterozygous deletion of chromosome 17p renders prostate cancer vulnerable to inhibition of RNA polymerase II. Nat Commun 2018;9(1):4394.
  • Nowsheen S, Aziz K, Aziz A, Deng M, Qin B, Luo K, Jeganathan KB, Zhang H, Liu T, Yu J, Deng Y, Yuan J, Ding W, van Deursen JM, Lou Z. L3MBTL2 orchestrates ubiquitin signaling by dictating the sequential recruitment of RNF8 and RNF168 after DNA damage. Nat Cell Biol 2018;20(4):455-464.
  • Wang L, Wang J, Xiong H, Wu F, Lan T, Zhang Y, Guo X, Wang H, Saleem M, Jiang C, Lu J, Deng Y. Co-targeting hexokinase 2-mediated Warburg effect and ULK1-dependent autophagy suppresses tumor growth of PTEN- and TP53-deficiency-driven castration-resistant prostate cancer. EBioMedicine, 2016;7:50-61.
  • Lei Wang, Hua Xiong, Fengxia Wu, Yingjie Zhang, Ji Wang, Liyan Zhao, Xiaolan Guo, Li-Ju Chang, Yong Zhang, M. James You, Shahriar Koochekpour, Mohammad Saleem, Haojie Huang, Junxuan Lu, Yibin Deng. Hexokinase 2-Mediated Warburg Effect Is Required for PTEN and p53-Deficiency Driven Prostate Cancer Growth. Cell Reports 2014; 8(5):1461-74.
  • An J, Wang C, Deng Y, Yu L, Huang H.Destruction of Full-Length Androgen Receptor by Wild-Type SPOP, but Not Prostate-Cancer-Associated Mutants.Cell Reports 2014;6(4):657-69.
  • Deng Y, Guo X, Ferguson DO, Chang S. Multiple roles of MRE11 at uncapped telomeres. Nature 2009; 460:914-8. See also Alt’s review “Mre11: roles in DNA repair beyond homologous recombination” in Nat Struct Mol Biol. 2009 Aug;16 (8):798-800 and Wu’s review “Identify crisis when telomeres left unprotected” in J Mol Cell Biol. 2010 Feb; 2(1): 14-6).
  • Yibin Deng and Sandy Chang. Telomere dysfunction and tumor suppression-the Senescence Connection. Nature Reviews Cancer 2008; 8(6):450-458.
  • Xiaolan Guo, Yibin Deng@, Yahong Lin, Wilfredo Cosme-Blanco, Suzanne Chan, Hua He, Guohua Yuan, Eric J. Brown, and Sandy Chang @ . Dysfunctional Telomeres Activate an ATM-ATR-Dependent DNA Damage Response to Suppress Tumorigenesis. EMBO J 2007; 26:4709-19 @Correspondence author.
  • Deng YB, Ren X, Yang L, Lin YH and Wu XW. A JNK-dependent pathway is required for TNF-induced apoptosis. Cell 2003,115:61-70; See review by Liu ZG “Adding facets to TNF signaling: The JNK angle” in Mol Cell. 2003; 12(4):795-6