Pu-Ste Liu
Assistant Professor

Assistant Professor Pu-Ste Liu

中文頁面

Address:
No.1, University Road, Tainan City 701, Taiwan (R.O.C.)
TEL (ext.):
5514 (Office), 5551 (Lab)
E-mail:
z11302014@ncku.edu.tw
Portrait of Assistant Professor Pu-Ste Liu

Education, Experience and Research

Education

  • Ph.D., Medical Sciences, National Cheng Kung University, Tainan, Taiwan (2003 – 2010)
  • M.S., Biochemistry and Molecular Biology, National Cheng Kung University, Tainan, Taiwan (2000 – 2002)
  • B.S., Medical Laboratory Science Biotechnology, China Medical University, Taichung, Taiwan (1996 - 2000)

Experience

  • Assistant Professor, Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan City, Taiwan (2024 - present)
  • Assistant Investigator, Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan (2018 – 2024)
  • Postdoctoral Fellow, Department of Fundamental Oncology, University of Lausanne, Ludwig Center for Cancer Research, Epalinges, Switzerland (2015 - 2018)
  • Postdoctoral Fellow, Department of Pharmacology, School of Medicine Minneapolis, University of Minnesota, MN, USA (2011 - 2014)
  • Postdoctoral Fellow, Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan (2010 - 2011)

Research Field

  • Immunology
  • Immunometabolism
  • Metabolic Syndrome
  • Cancer Immunotherapy

Research Interests

Our research investigates the role of macrophage immunometabolism in regulating chronic inflammatory diseases and disease progression, with particular emphasis on metabolic syndrome (type 2 diabetes, insulin resistance, and atherosclerosis) and cancer. Using an integrated approach of transcriptomics, metabolomics, and epigenomics, we aim to clarify the metabolic checkpoints and regulatory molecular mechanisms that affect macrophage activation and function during disease progression. We focus in particular on the immunometabolic mechanisms that dysregulate macrophages in disease microenvironments, such as the adipose tissue of diabetic patients, the arterial microenvironment in atherosclerosis, and tumor tissue. We are committed to understanding how immunometabolism affects the function of adipose tissue macrophages, atherosclerotic macrophages, and tumor-associated macrophages under these disease conditions, and we intend to target the immunometabolic circuits of these macrophages in order to improve macrophage immunity and function and thereby improve disease outcomes.

Our two main current research directions are:

  1. Mechanisms of trained immunity in obesity and obesity-induced atherosclerosis
  2. Deciphering how mitochondria regulate the immune responses and functions of tumor-associated macrophages

Publications

  1. Liu PS*, Chen YT, Li XY, Hsueh PC, Tzeng SF, Shi PZ, Xie X, Parik S, Fendt S-M, Ho PC*. CD40 signal rewires fatty acid and glutamine metabolism for stimulating macrophage anti-tumorigenic functions. Nature Immunology, 2023, 24, 452-62.
  2. Raines LN, Zhao H, Wang Y, Chen H-Y, Gallart-Ayala H, Hsueh P-C, Cao W, Koh Y, Alamonte-Loya A, Liu PS, Ivanisevic J, Lio C-WJ, Ho P-C, Huang SC-C. PERK is a critical metabolic hub for immunosuppressive function in macrophages. Nature Immunology, 2022, 23, 431–445.
  3. Yu YR, Imrichova H, Wang H, Chao T, Xiao Z, Gao M, Rincon-Restrepo M, Franco F, Genolet R, Cheng WC, Jandus C, Coukos G, Jiang YF, Locasale JW, Zippelius A, Liu PS, Tang L, Bock C, Vannini N, Ho PC. Disturbed mitochondrial dynamics in CD8+ TILs reinforce T cell exhaustion. Nature Immunology, 2020, 21, 1540–1551.
  4. Xie X, Liu PS, Percipalle P. Analysis of global transcriptome change in mouse embryonic fibroblasts after dsDNA and dsRNA viral mimic stimulation. Frontiers in Immunology, section Molecular Innate Immunity, 2019, 10, 836.
  5. Liu PS, Ho PC. Determining macrophage polarization upon metabolic perturbation. Methods in Molecular Biology, 2018; 1862; 173-186.
  6. Liu PS*, Ho PC. Mitochondria: A master regulator in macrophage and T cell immunity. Mitochondrion, 2018; 41; 45-50.
  7. Lin YW, Liu PS, Pook KA, Wei LN. Glyburide and retinoic acid synergize to promote wound healing by anti-inflammation and RIP140 degradation. Scientific Reports, 2018; 8; 834.
  8. Liu PS, Wang HP, Li XY, Chao T, Teav T, Christen S, Di Conza G, Chen WC, Chou CH, Vavakova M, Muret C, Debackere K, Mazzone M, Hung HD, Maria-Fendt S, Ivanisevic J, Ho PC. Integration of α-ketoglutarate/succinate balance controls macrophage polarization through immunometabolic and epigenetic reprogramming. Nature Immunology, 2017; 18; 985-994.
  9. Ho PC, Liu PS. Metabolic communication in tumors: a new layer of immunoregulation for immune evasion. Journal for Immunotherapy of Cancer, 2016; 4: 4.
  10. Lin YW, Lee B, Liu PS, Wei LN. Receptor-interacting protein 140 orchestrates the dynamics of macrophage M1/M2 polarization. Journal of Innate Immunity, 2016; 8: 97-107.
  11. Liu PS, Lin YW, Burton FH, Wei LN. Injecting engineered anti-inflammatory macrophages therapeutically induces white adipose tissue browning and improves diet-induced insulin resistance. Adipocyte, 2015; 4: 123-128.
  12. Liu PS, Lin YW, Burton FH, Wei LN. M1-M2 balancing act in white adipose tissue browning – a new role for RIP140. Adipocyte, 2015; 4: 146-148.
  13. Lin YW, Liu PS, Adhikari N, Hall JL, Wei LN. RIP140 contributes to foam cell formation and atherosclerosis by regulating cholesterol homeostasis in macrophages. Journal of Molecular and Cellular Cardiology, 2015; 79: 287-294.
  14. Liu PS, Lin YW, Lee B, McCrady-Spitzer SK, Levine JA, Wei LN. Reducing RIP140 expression in macrophage alters ATM infiltration, facilitates white adipose tissue browning and prevents high fat diet-induced insulin resistance. Diabetes, 2014; 63: 4021-4031.
  15. Liu PS, Jong TH, Maa MC, Leu TH. The interplay between Eps8 and IRSp53 contributes to Src-mediated transformation. Oncogene, 2010; 29: 3977-89.
  16. Shiau AL, Liu PS and Wu CL. Novel strategy for generation and titration of recombinant adeno-associated virus vectors. Journal of Virology, 2005; 79: 193-201.