Peng Jiang Ph.D
Associate Professor
1999-2003 B.S., Anhui University, School of Life Sciences.
2003-2008 Ph.D., University of Science and Technology of China, School of Life Sciences.
2008-2013 Postdoc, University of Pennsylvania, Perelman School of Medicine.
2013-2014 Research Associate, University of Pennsylvania, School of Medicine.
2014-2021 Tenure-track Assistant Professor, Tsinghua University, School of Life Sciences.
2020- Principal Investigator, Tsinghua-Peking Center for Life Sciences
2021- Associate Professor, Tsinghua University, School of Life Sciences.
Research interest
The Jiang laboratory is interested in tumor and immune cell metabolism.
The metabolism inside and outside tumor cells is markedly different from that of normal cells in differentiated tissues. Metabolic reprogramming typically confers a pro-proliferative and/or survival advantage to tumor cells. Emerging evidence suggests that metabolic alterations are ultimately linked to genetic changes that contribute to cell fate decisions. Tumor development is thought to be driven by intrinsic factors, but the extrinsic microenvironment also has an impact.
Currently, the lab focuses on two related areas: 1) Tumor metabolism. How cancer cells reprogram their metabolism, with special reference to the role of p53, and the urea cycle metabolism in tumor development. Through systematic studies, we wish to gain a clear understanding of the relationship between metabolism and the nature of tumors; 2) Immune cell metabolism in the microenvironment. We are particularly interested in how immune cells sense changes in nutrients or microenvironmental metabolites and how metabolic remodeling affects anti-tumor immune responses. Understanding these issues will not only be of great value in identifying and targeting therapeutic windows for cancer, but may also provide insights into the evolutionary mechanisms of tumors.
The major findings of Jiang lab in the past few years include: 1) malignant tumors carrying p53 deletions or mutations have abnormally altered metabolic pathways such as NADPH, polyamine and the urea cycle metabolic pathways, 2) tumor cell proliferation and survival are heavily dependent on the up-regulation of polyamine synthesis and one-carbon metabolism, and 3) specific metabolites/amino acids in the intracellular or microenvironmental context, such as citrulline, fumarate, asparagine, and 2-hydroxyglutarate (2-HG), can be sensed by tumor or immune cells, and significantly affect immune response and anti-tumor capacity.
Selected publications
1. Xu X, Wang J, Xu L, Li P*, Jiang P*. p53 suppresses lipid droplet-fueled tumorigenesis through phosphatidylcholine. J Clin Invest. 2024 Jan 9;134(4).
2. Chen T#, Xie S#, Cheng J, Zhao Q, Wu H*, Jiang P*, Du W*. AKT1 phosphorylation of cytoplasmic ME2 induces a metabolic switch to glycolysis for tumorigenesis. Nat Communs. (2024) Jan 23;15(1):686.
3. Xia W, Jiang P*. p53 promotes antiviral innate immunity by driving hexosamine metabolism. Cell Reports. (2024) Jan 30;43(2):113724.
4. Cheng J#, Yan J#, Liu Y#, Shi J#, Wang H, Zhou H, Zhou Y, Zhang T, Zhao L, Meng X, Gong H, Zhang X*, Zhu H*, Jiang P*. Cancer-cell-derived fumarate suppresses the anti-tumor capacity of CD8+ T cells in the tumor microenvironment. Cell Metabolism. (2023) Jun 6;35(6):961-978.
5. Cheng, J#, Liu, Y#, Yan, J#, Zhao L, Zhou Y, Shen X, Y, Chen Y, Meng X, Zhang X* & Jiang P*. Fumarate suppresses B-cell activation and function through direct inactivation of LYN. Nature Chemical Biology (2022). Sep;18(9):954-962.
6. Zhao M#, Yao P#, Mao Y#, Wu J#, Wang W, Geng C, Cheng J, Du W * and Jiang P*. Malic enzyme 2 maintains protein stability of mutant p53 through 2-hydroxyglutarate. Nature Metabolism. (2022). Feb;4(2):225-238.
7. Mao Y, Shi D, Li G, Jiang P*. Citrulline depletion by ASS1 is required for proinflammatory macrophage activation and immune responses. Molecular Cell. (2022) Feb 3;82(3):527-541.
8. Li G#, Wu J#, Li L, Jiang P*. p53 deficiency induces MTHFD2 transcription to promote cell proliferation and restrain DNA damage. Proc Natl Acad Sci U S A. (2021) Jul 13;118(28)
9. Wu J#, Li G#, Li L, Li D, Dong Z, Jiang P*. Asparagine enhances LCK signalling to potentiate CD8+ T cell-activation and anti-tumour responses. Nature Cell Biology, (2021) 23(1):75-86.
10. Deng L, Yao P, Li L, Ji F, Zhao S, Xu C, Lan X, Jiang P*. p53-mediated control of aspartate-asparagine homeostasis dictates LKB1 activity and modulates cell survival. Nature Communs, (2020) 11, 1755-18;
11. Li L, Mao Y, Zhao L, Li L, Wu J, Zhao M, Du W, Yu L, Jiang P*. p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis. Nature. (2019) 567(7747):253-256.
12. Li L#, Li L#, Li W, Chen T, Bin Zou, Zhao L, Wang H, Wang X, Xu L, Liu X, Wang D, Li B, Mak TW, Du W*, Yang X*, Jiang P*. TAp73-induced phosphofructokinase-1 transcription promotes the Warburg effect and enhances cell proliferation. Nature Communs. (2018), Nov 8; 9(1):4683.
13. Du W#, Jiang P#, Mancuso A, Stonestrom A, Brewer M, Minn AJ, Mak TW, Wu M* and Yang X*. TAp73 enhances the pentose phosphate pathway and supports cell proliferation. Nature Cell Biology. (2013), Aug. 15, 991–1000.
14. Jiang P#, Du W#, Mancuso A, Wellen KE, Yang X*. Reciprocal regulation of p53 and malic enzymes modulates metabolism and senescence. Nature. (2013), Jan. 493: 689-693.
15. Jiang P#, Du W#, Wang X, Mancuso A, Gao X, Wu M* and Yang X*. p53 regulates biosynthesis through direct inactivation of glucose-6-phosphate dehydrogenase. Nature Cell Biology. (2011) Mar.13: 310-316.
Contact information
Email: pengjiang@mail.tsinghua.edu.cn
Phone:010-62786079 (Office), or 010-62783063 (Laboratory)
Mail: Rm E105, Biomedical Building, Tsinghua University, Haidian District, Beijing, China, 100084
http:/lifeen/info/1032/1070.htm or http://www.cls.edu.cn/english/PrincipalInvestigator/pi/index4821.shtml
