Zeng Musheng
Vice-President
Experimental Research
Sun Yat-sen University Cancer Center
China
Biography
Prof. Musheng Zeng is a vice director and professor of Sun Yat-sen University Cancer Center. He gained his Ph.D. degree at Sun Yat-sen University in 1998 and had his Post-doc training in Tennessee State University and New England Medical Center, Tufts University from 1999 to 2003. Prof. Musheng Zeng moved back to China to start his lab since 2003. In 2014, he was awarded as Changjiang Scholar Professor from Ministry of Education of China. Zeng's laboratory majorly engages in the pathogenesis and etiology of Nasopharyngeal Carcinoma (NPC), especially the mechanism of EBV infection and transformation in nasopharyngeal epithelial cells. In endemic regions, NPC presents as a complex disease caused by an interaction of Epstein-Barr virus (EBV) chronic infection, environmental, and genetic factors, in a multistep carcinogenic process.
Research Interest
Prof. Zeng has previously deeply studied the variation of EBV and completed the first full-length genomic sequence analysis of an NPC-derived EBV strain (termed GD1, Guangdong strain 1). He has already established the first cellular proto-oncogene immortalized nasopharyngeal epithelial cell line and preliminarily illuminated the mechanisms involved in the tumorigenesis of NPC, and found the functional and mechanistic links between the oncoprotein Bmi-1 and the tumor suppressor PTEN in the development and progression of cancer. Most importantly, he recently established highly infective efficiency and stable in vitro epithelial cell model for EBV infection. Moreover, he discovered that EBV encoded LMP2A could induce epithelial mesenchymal transition (EMT) and increases side population of stem-like cancer cells in NPC, suggesting a novel mechanism by which EBV induces the initiation, metastasis and recurrence of NPC. Recently, he has identified that NRP1 interacts with gB and mediates EBV infection of nasopharyngeal epithelial cells, putting forward the novel mechanism of EBV infecting epithelial cells.