系统生物医学学者讲坛第十一期：Targeting Cell SignalingPathways for Cancer Therapies  

主讲人：Professor Wei, Wenyi

       Department of Pathology, Beth Israel Deaconess MedicalCenter, Harvard Medical School

EducationBackground:

2002 PhD in Molecular Biology& Cell Biology and Biochemistry, Brown University, Providence, RI   

1996 M.S. inBiochemical Engineering, Chinese Academy ofSciences, Beijing, P.R. China   

1993 B.A.in Microbiology, Shandong University, Jinan, P.R. China,   

Positions:

2015- Director,Biochemistry Program, BIDMC Cancer Center and Cancer Research Institute,Boston, MA   

2007- AssociateMember, Biological and Biomedical Sciences Graduate Program, Harvard MedicalSchool, Boston, MA   

March 2017 Professor,Dept. of Pathology, Beth Israel Deaconess Medical Center, Harvard MedicalSchool, Boston, MA   

2012- 2017 AssociateProfessor, Dept. of Pathology, Beth Israel Deaconess Medical Center, HarvardMedical School, Boston, MA   

Oct. 2006-2012 AssistantProfessor, Dept. of Pathology, Beth Israel Deaconess Medical Center, HarvardMedical School, Boston, MA   

2005-Oct. 2006 Instructorin Medicine, Harvard Medical School, Boston, MA (Mentor, Dr. William G. Kaelin,Jr.)   

2002- 2005 Research Associate, Departmentof Medical Oncology, Dana Farber Cancer Institute, Boston, MA (Mentor, Dr.William G. Kaelin, Jr.)   

Personal Statement:

My laboratory mainlyfocuses on understanding mechanistically how aberrant cell signaling eventslead to altered protein homeostasis and cellular functions to facilitate thedevelopment of human disorders including cancer. Our research is uniquelypoised to understand how post-translational modifications including lysineubiquitination, acetylation and methylation generate a complex coding system totransduce cellular messages, and crosstalk with other signaling pathways, suchas well-studied kinase-cascades, to govern various cellular processes. One ofthe major focus lies in understanding how aberrant cell cycle regulation leadsto cancer development. To this end, proper cell cycle transitions are largelydriven by waves of ubiquitin-dependent degradation of key cell cycle regulatorsby APC or SCF, the two major E3 ligase complexes. Thus one of the main researchfocus in my laboratory at Department of Pathology, BIDMC is focused onunderstanding how APC and SCF activities contribute towards cell cycle regulationand subsequent tumor formation. I will present new information regarding ourdedicated efforts in utilizing multidisciplinary approaches includingbiochemical and genetic analysis to understand the tumor suppressor role ofCdh1 or Fbw7 and the oncogenic potential of Skp2, as well as in defining themolecuar mechanisms underlying how frequent activaiton of the PI3K/Akt/mTORonogenic signaling pathway drives tumoirgenesis. These results will help tobetter understand the multilayer regulation of the delicate network ofsignaling pathways and their physiologica contribution to cancer development,which will lead us to the design of more efficient intervention strategies tocombat cancer and other diseases.