BS, Fudan University, Shanghai, China 1981
PhD. Columbia University, New York, NY, 1988
Mechanisms of metastasis
My laboratory has been interested in the molecular mechanism of tumor cell invasion by focusing on the regulation of actin polymerization, the driving force that facilitates the formation of membrane protrusions and the penetration of tumor cells into extracellular matrix. In particular, we have been studying on cortactin, a gene that plays a critical role in the regulation of the assembly of actin filaments within the area for cellular protrusion. Our study has found that overexpression of cortactin, which occurs in many types of cancers as a result of gene amplification, enhances metastasis. More recent study demonstrates that cortactin regulates cell motility and invasion by promoting membrane remodeling as well as intracellular trafficking of internalized receptors. The current work is focusing on the mechanism to regulate the function of cortactin by Src oncogene. We are also investigating a new cortactin binding protein, missing in metastasis (MIM), a gene that is frequently down regulated in advanced bladder carcinomas and modulates the motility of cells induced by extracellular agonists. The current research goal is to reveal the physiological and pathological role of MIM in cells and tumor invasion.
Lin,J., Liu,J., Wang,Y., Zhu,J., Zhou,K., Smith,N., and Zhan,X. (2005). Differential regulation of cortactin and N-WASP-mediated actin polymerization by missing in metastasis (MIM) protein. Oncogene 24, 2059-2066.
Zhu,J., Zhou,K., Hao,J.J., Liu,J., Smith,N., and Zhan,X. (2005). Regulation of cortactin/dynamin interaction by actin polymerization during the fission of clathrin-coated pits. J. Cell Sci. 118, 807-817.
Hao, JJ., Zhu, J., Zhou, K., Smith, E., and Zhan, X. (2005) The coiled-coil domain is required for HS1 to bind to F-actin and activate Arp2/3 complex. J. Biol. Chem. 280, 37988-37994.
Wang,Y., Liu,J., Zhou,K., Smith,E., and Zhan,X. (2006). Association of poor expression of missing in metastasis gene with undifferentiation of bladder transitional carcinoma. Cancer Res. Cancer Investigation (In press)