1983毕业于年在南昌大学生物系，1989年获中国科学院遗传研究所硕士学位；1997年于美国南卡罗来纳大学获分子遗传学博士学位；1997年－2002年在美国加州大学洛杉矶分校Cedar-Sinai医学中心从事博士后研究工作。2002年－2004年在美国加州大学洛杉矶分校医学院担任助理教授。 2004年7月由中国科学院“百人计划”引进回国。任肿瘤分子生物学课题组组长。近年来的主要研究方向为肿瘤发生与转移的分子机制，利用分子、细胞生物学方法及多种动物模型研究与肿瘤发生与转移的相关蛋白之间的相互作用及其信号转导，揭示肿瘤发生与转移的分子基础。近年来在Cancer Cell, Immunity, Nature Commmunication, Gastroenterology, Hepatology, Cancer Research, Oncogene等国际学术期刊上发表研究论文80余篇, 目前担任国际杂志《Journal of Biological Chemistry》,《Journal of Cell Communication and Signaling》和《Molecular Nutrition Food Research》编委。
The action and activity of proteins in cancerous cells is an area of study that has provided us with many therapeutic targets. However, the targeted activation of tumor-suppressor proteins has not been readily achieved in the clinic. here, research into EphB3, a protein that is overexpressed in non-small-cell lung cancer (NSCLC), has led to the surprising discovery that phosphorylation of this protein by EphB3 kinase 'turns' it into a tumor-suppressor protein. we find that the expression of its cognate ligands, either ephrin-B1 or ephrin-B2, is significantly downregulated, leading to reduced tyrosine phosphorylation of EphB3. Forced activation of EphB3 kinase in EphB3-overexpressing non-small-cell lung cancer cells inhibits cell migratory capability in vitro as well as metastatic seeding in vivo. Furthermore, we identify a novel EphB3-binding protein, the receptor for activated C-kinase 1, which mediates the assembly of a ternary signal complex comprising protein phosphatase 2A, Akt and itself in response to EphB3 activation, leading to reduced Akt phosphorylation and subsequent inhibition of cell migration. Our study reveals a novel tumour-suppressive signalling pathway associated with kinase-activated EphB3 in non-small-cell lung cancer, and provides a potential therapeutic strategy by activating EphB3 signalling, thus inhibiting tumour metastasis.