Qunying LEI
M.D. &Ph.D, Professor
E-mail: qlei@fudan.edu.cn
 


EDUCATION

1999-2002    Ph.D. Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, China

1996-1999    M.S. Department of Biochemistry and Molecular Biology, Suzhou University, China

1988-1993    B.S. (M.D.) Public Health, Jiangxi Medical College, China


EMPLOYMENTS

2017-Present    Professor, Shanghai Cancer Center and Institute of Biomedical Sciences, Fudan University, China

2009-2016        Professor, Basic Medical College and Institute of Biomedical Sciences, Fudan University, China

2006-2009        Associate Professor, Basic Medical College and Institute of Biomedical Sciences, Fudan University, China

2003-2006        Postdoctoral Researcher, Prof. Hong Wu’s Laboratory, Department of Molecular and Medical Pharmacology, University of California, Los Angeles, CA UCLA

2002-2003        Postdoctoral Researcher, Prof. Robert H Lane’s Laboratory, Department of Pediatric, School of Medicine, U.S.A


KEY RESEARCH ACHIVEMENT

Prof. Lei’s study focuses on exploring cell metabolism and its dysregulation in cancer development. Her research work finds that post translational modifications of critical metabolic enzymes, like acetylation of M2 Isoform of pyruvate kinase (PKM2) and lactate dehydrogenase A (LDHA) in glycolysis, ATP- citrate lyase (ACLY) in lipid Biosynthesis, methionine adenosyltransferase IIα (MAT IIα) in the methionine cycle, and others, regulate enzymatic activity and protein stability under different metabolic stress and play essential role in tumor development. Moreover, her work reveals that arginine at different metabolic enzymes, including malate dehydrogenase 1 (MDH1), SIRT7 as well as GAPDH is critical to sense various nutrient/metabolites flux to regulate physiological or pathological processes, like mitochondria biogenesis, redox homeostasis. Notably, Prof. Lei’s et al identified that LDHA functions as ROS sensor and moves into nucleus, followed by obtaining non-canonical enzymatic activity to produce α-hydroxybutyrate and epigenetically activate expression of antioxidant response genes in HPV-induced cancers. Furthermore, her recent study deciphers the BCAA-BCAT2 catabolism drives PDAC development, which significantly impeded by using BCAT2 inhibitor or BCAA restriction in animal model. Altogether, these studies broaden our understanding on metabolite/nutrition sensing and their critical role in tumor initiation and progression, and enable us to design precision therapy by targeting metabolic vulnerability specifically rewired in cancers.


WORK FOR PROFESSIONAL SOCIETIES

2014-Present   Committee of Chinese Society of Biochemistry and Molecular Biology (CSBMB)       

2014-Present   Committee of Chinese Society for Cell Biology (CSCB),

2015-Present   Associate Director of Chinese Society of Medical Biochemistry and Molecular Biology, CSBMB

2015-Present   Associate Director and Secretary General of Shanghai Society for Biochemistry and Molecular Biology,

2018-Present   Director of Chinese Society for cell metabolism, CSCB


Research Focus:

1.    Nutrition/metabolite sensing and cell metabolism;

2.    Metabolic plasticity in cancer cells;

3.    Tumor metabolism and tumor microenvironment.