College of Basic Medical Sciences


ZHU Liang

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Tel: +86-21-54561329

Research Field: Cancer Pharmacology and Metabolomics

Personal Introduction

  • The lack of new drug targets for molecularly-targeted therapy and immunotherapy and the emergence of resistance are bottlenecks in cancer science and clinical practice. We pursue an exploration of the mechanisms of tumor initiation, progression and therapy resistance, from a new angle, using the team-built metabolomics-based integrated multiomics analysis. By this strategy, we aim to discover novel therapeutic targets and therapy resistance-overcoming targets, as well as to the research and development of new anticancer drugs. The findings have been published in top science journals such as Science Translational Medicine and Cell Metabolism and undergone the translational process.

  • Liang ZHU received his Bachelor degree and Master degree in 1997 and 2000, respectively. Then he entered Shanghai Jiao Tong University School of Medicine as a teaching assistant and a lecturer. In 2007, he obtained PhD in Pharmacology in the University. During 2008 and 2010, he performed postdoctoral fellowship at Institute of Biology Valrose Centre National de la Recherche Scientifique (CNRS) in France. Liang ZHU is now a professor of Pharmacology and the executive deputy director of Department of Pharmacology and Chemical Biology at the Shanghai Jiao Tong University School of Medicine. He is also the Principal Investigator of Group Cancer Pharmacology and Metabolomics.


  • Zhang, K.R., et al (2021). Targeting AKR1B1 inhibits glutathione de novo synthesis to overcome acquired resistance to EGFR targeted therapy in lung cancer. Sci Trans Med. 13(614): eabg6428(Last corresponding author)

  • Ma, C. S., et al. (2021). “NRF2-GPX4/SOD2 axis imparts resistance to EGFR-tyrosine kinase inhibitors in non-small-cell lung cancer cells.” Acta Pharmacol Sin. 42: 613-23(Last corresponding author)

  • Lv, Q.-M., et al. (2021). "Cancer cell-autonomous cGAS-STING response confers drug resistance." bioRxiv(Last corresponding author)

  • Zhang, Y. F., et al. (2020). "Development and validation of a rapid, robust and sensitive UPLC-QQQ-MS/MS method for simultaneous quantification of GSH metabolism in lung cancer cells." J Chromatogr B. 1148: 122145(Last corresponding author)

  • Lei, H. M., et al. (2019). "Aldehyde dehydrogenase 1A1 confers erlotinib resistance via facilitating the reactive oxygen species-reactive carbonyl species metabolic pathway in lung adenocarcinomas." Theranostics. 9(24): 7122-7139(Last corresponding author)

  • Liang, Q., et al. (2021). "HKB99, an allosteric inhibitor of phosphoglycerate mutase 1, suppresses invasive pseudopodia formation and upregulates plasminogen activator inhibitor-2 in erlotinib-resistant non-small cell lung cancer cells." Acta Pharmacol Sin. 42: 115-19(Co-corresponding author)

  • Dong, J., et al. (2018) Overcoming erlotinib resistance in EGFR mutation–positive lung adenocarcinomas through repression of phosphoglycerate dehydrogenase. Theranostics. 8:1808-23(Co-corresponding author)

  • Tang, Y., et al. (2022). "Metabolomics analysis reveals Oct4 overexpression drives metabolic reprogramming and enhanced glycolysis and pentose phosphate pathway in lung adenocarcinoma cells." Biomed Chromatogr 36(6): e5367

  • Wang, Y., et al. (2019). "UPLC-MS-based metabolomics reveals metabolic dysregulation in ALDH1A1-overexpressed lung adenocarcinoma cells." Metabolomics 15(4): 52

  • Xu, Y., et al. (2022). "The KRAS-G12D mutation induces Metabolic Vulnerability in B-cell Acute Lymphoblastic Leukemia." iScience: 103881

  • Huang, K., et al. (2019). "A Novel Allosteric Inhibitor of Phosphoglycerate Mutase 1 Suppresses Growth and Metastasis of Non-Small-Cell Lung Cancer." Cell Metab 30(6): 1107-1119

  • Liu, X., et al. (2018). "PPM1K Regulates Hematopoiesis and Leukemogenesis through CDC20-Mediated Ubiquitination of MEIS1 and p21." Cell Rep 23(5): 1461-1475

  • Ma, P., et al. (2017). "Simultaneous evolutionary expansion and constraint of genomic heterogeneity in multifocal lung cancer." Nat Commun 8(1): 823