Dr. Lianfeng WU received his Ph.D. in Biochemistry and Molecular Biology from the Institute of Biophysics, Chinese Academy of Sciences in 2010. From 2011 to 2017, he worked at Harvard Medical School and Massachusetts General Hospital and was promoted to be an Instructor of Harvard Medical School in 2017. In September of 2017, Dr. Wu joined Westlake University as an Assistant Professor.

With the central goal to promote human health and life, Dr. Wu’s research focused on studies of mechanisms by which well-known protein molecules and therapeutic drugs exert health-promoting effects. Dr. Wu is well recognized by his Ph.D. work on the function characterization of granzymes, a group of protein molecules used by human immune system to kill cancer and viral-infected cells, the determination of human granzyme M structure, and the design of its specific inhibitor. These work have been published in some of the best biomedical journals, including The Journal of Immunology, Cell Death & Differentiation, and Journal of Biological Chemistry. For his postdoctoral study, Dr. Wu used a variety of approaches to solve a 60-year mystery in medicine: the mode of action of the antidiabetic drug metformin. Metformin is one of the most widely therapeutic agents to treat type 2 diabetes, but it also appears to have far reaching health benefits including decreased incidence of certain cancers and promoting lifespan in model organisms. His postdoctoral work was published as the “Featured Article” in Cell and recognized as the best basic science manuscript from all of Massachusetts General Hospital in 2016. In that work, he detailed completely new aspects of the biological response to metformin, particularly with regard to the genetic pathways necessary for metformin to prolong lifespan and kill cancer cells. Currently, Dr. Wu’s Lab continue studying the underlying mechanisms how human aging and metabolic disorders occur by leveraging the integrated power of genetics, biochemistry and physiology in varied systems, including the nematode C. elegans, cultured cells and mouse model.

1.  Webster CM, Pino EC, Carr CE,Wu L, Zhou B, Cedillo L, Kacergis MC, Curran SP, Soukas AA. Genome-wide RNAi Screen for Fat Regulatory Genes in C. elegans Identifies a Proteostasis-AMPK Axis Critical for Starvation Survival.Cell Rep. 2017, 20 (3): 627-640.

2.  Wu L, Zhou B, Oshiro-Rapley N, Li M, Paulo JP, Webster CM, Mou F, Kacergis MC, Talkowski ME, Carr CE, Gygi SP, Zheng B, Soukas AA. An ancient, unified mechanism for metformin growth inhibition in C. elegans and cancer.Cell.2016, 167 (7), 1705-1718. Designated as “Featured Article” with a Preview  and also highlighted as an “Editor’s Choice” in Science Signaling.

3.  Webster CM,Wu L, Douglas D, and Soukas AA. A non-canonical role for the C. elegans dosage compensation complex in growth and metabolic regulation downstream of TOR complex 2.Development. 2013, 140(17): 3601-36012.

4.  Wang L, Li Q, Wu L, Liu S, Zhang Y, Yang X, Zhu P, Zhang H, Zhang K, Lou J, Liu P, Tong L, Sun F, and Fan Z. Identification of SERPINB1 as a physiological inhibitor of human granzymeH. J Immunol. 2013, 190(3): 1319-1330;

5.  Yuan M, Pino E,Wu L, Kacergis M, and Soukas AA. Identification of Akt-independent regulation of hepatic lipogenesis by mammalian target of rapamycin (mTOR) complex 2.J Biol Chem. 2012, 287(35): 29579-2988;

6.  Wang L, Zhang K,Wu L, Liu S, Zhang H, Zhou Q, Tong L, Sun F, and Fan Z. Structural insights into the substrate specificity of human granzyme H: the functional roles of a novel RKR motif.J Immunol. 2012, 188(2): 765-773;

7.  Hu D, Liu S, Shi L, Li C,Wu L, and Fan Z. Cleavage of survivin by Granzyme M attenuates its stability and impairs its cytoprotective function.J Biol Chem. 2010, 285(24): 18326-18335;

8.  Wu L, Wang L, Hua G, Liu K, Yang X, Zhai Y, Bartlam M, Sun F, and Fan Z. Structural basis for proteolytic specificity of the human apoptosis-inducing granzyme M.J Immunol. 2009, 183(1): 421-429;

9.  Shi L,Wu L, Wang S, and Fan Z. Granzyme F induces a novel death pathway characterized by Bid-independent cytochrome c release without caspase activation.Cell Death Differ. 2009, 16(12): 1694-1704.