Lei Jiang, Ph.D.
- Assistant Professor, Molecular & Cellular Endocrinology
Lei Jiang, Ph.D.
Research Focus :
- Molecular and Cellular Endocrinology
- Metabolic Alteration in Obesity and Diabetes
- Central Carbon Metabolism in Cancer
- Systemic Metabolic Flux Analysis
Other Languages Spoken
Lei Jiang received his bachelor's degree from Wuhan University, and then completed his Ph.D. at Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, where he received the Dean Award and Unilever Scholarship, and he was also honored as a Merit student.
After his postdoctoral training in University of Texas Southwestern Medical Center at Dallas, he joined City of Hope as an assistant professor in the department of Molecular & Cellular Endocrinology. During his research training, Dr. Jiang has had several high-profile publications in Nature, Nature Cell Biology, Cell, Molecular Cell, Hepatology, PNAS and Metabolic Engineering. His research interest is to elucidate the molecular mechanisms regulating nutrient homeostasis during the development and progress of metabolic diseases such as diabetes and cancer.
His research particularly focuses on the compartmentalized central carbon metabolism (glycolysis and oxidative phosphorylation) under pathological conditions, through the application of the leading- edge mass spec based metabolic tracing and systemic bioengineering.
- 2009, Ph.D., Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
- 2004, B.S. , Wuhan University, Wuhan, China
- 2009-2016, UT Southwestern Medical Center, Dallas, TX
Metabolism is a fundamental biological phenomenon. Dysregulated metabolism contributes to a variety of disease, including cancer and diabetes, which are known as metabolic disease. Metabolic alteration has been studied at several levels, from the whole organism to the single cells and subcellular organelles. The balance between energy intake and energy expenditure controls the body weight gain; while all the organs in our body have their own metabolic feature. Each organ contains several kinds of cell types with different metabolism, and tumor is also famous for its metabolic heterogeneity. Even within the cells, all kinds of nutrient are used to provide the support for basic cellular activities, including survival, mobility and growth.
A major goal of my research is to explore the coordinated metabolic adaptation under both normal physiological and specific pathological conditions. Metabolic reactions have their spatial and temporal distribution, which is also known as cellular compartmentation. A wide variety of cell types present in both the adipose tissue of diabetic patients and the tumor of cancer patients, and their metabolism actively communicates with each other, which is another layer of compartmentation. Metabolites, like citrate and serine, are well known for their nutrient role, and they can also serve as signal molecule between the cells and within the subcellular structure. My recent study showed that a novel cytosol-to-mitochondria citrate transport system mitigates the mitochondrial oxidative stress in the detached cancer cell, and we will look into the signaling control between the subcellular organelles.
With the aim of precision medicine, biology becomes a data-rich science. While the genetic heterogeneity is widely accepted with the easy access to the large sequencing data, the metabolic heterogeneity has also been more appreciated with the evolution of the analytical tools. The integration of mass spec based metabolic tracing and mathematical bioengineering based modeling prediction will provide a new angle to understand the metabolic rewiring in diabetes, cancer and other diseases. A better knowledge of the central carbon metabolism, amino acid utilization and nucleic acid synthesis will lead to new diagnostic approach and potential novel drug target.
- Jiang L, Boufersaoui A, Yang C, Ko B, Rakheja D, Guevara G, Hu Z, DeBerardinis RJ. Quantitative metabolic flux analysis reveals an unconventional pathway of fatty acid synthesis in cancer cells deficient for the mitochondrial citrate transport protein. Metab Eng. 2017
- Jiang L, Shestov AA, Swain P, Yang C, Parker SJ, Wang QA, Terada LS, Adams ND, McCabe MT, Pietrak B, Schmidt S, Metallo CM, Dranka BP, Schwartz B, DeBerardinis RJ. Reductive carboxylation supports redox homeostasis during anchorage-independent growth. Nature. 2016
- Jiang L, Xiao L, Sugiura H, Huang X, Ali A, Kuro-o M, Deberardinis RJ, Boothman DA. Metabolic reprogramming during TGFβ1-induced epithelial-to-mesenchymal transition. Oncogene. 2015
- Schell JC, Olson KA, Jiang L, Hawkins AJ, Van Vranken JG, Xie J, Egnatchik RA, Earl EG, DeBerardinis RJ, Rutter J. A role for the mitochondrial pyruvate carrier as a repressor of the Warburg effect and colon cancer cell growth. Mol Cell. 2014
- Yang C, Ko B, Hensley CT, Jiang L, Wasti AT, Kim J, Sudderth J, Calvaruso MA, Lumata L, Mitsche M, Rutter J, Merritt ME, DeBerardinis RJ. Glutamine oxidation maintains the TCA cycle and cell survival during impaired mitochondrial pyruvate transport. Mol Cell. 2014
- 2017-present, American Diabetes Association
- 2015-present, American Association for Cancer Research
- 2015, Travel Award for Poster Presentation, UTSW, Dallas, TX
- 2009, Unilever Scholarship, China
- 2009, Chinese Academy of Sciences Dean Award, China
- 2008, Merit student, Chinese Academy of Sciences, China