报告题目：Role of Phosphatidylinositol-4,5-bisphosphate signaling in cancer progression
报告人： Kun Ling, Associate Consultant, Assistant Professor, Department of Biochemistry and Molecular Biology, Mayo Clinic Cancer Center.
主持人： 王平教授
报告时间：9月21日 13:30（周五）
报告地点：闵行生命科学学院大楼534报告厅
报告人简介：Kun Ling博士，1996年获得中国海洋大学本科学位，2001年获得中科院生化所分子细胞生物学博士学位，之后到美国威斯康星大学医学院药理学系做博士后研究，2005年起任该部门助理研究员，2007年11月起任美国梅奥医学癌症中心生物化学与分子生物学部门助理顾问、助理教授。
报告内容简介：Phosphatidylinositol-4,5-bisphosphate (PtdIn4,5P2) is a lipid second messenger playing multiple roles throughout the cell. Along with others'' findings, our previous and recent results suggest that PtdIn4,5P2 signaling involves in centriole duplication, E-cadherin transport and assembly, actin reorganization, focal adhesion turnover, and cell migration and invasion. All these events are related to cancer initiation and progression. Indeed, we found that depletion of type Igamma phosphatidylinositol phosphate kinase (PIPKIgamma) that generates PtdIn4,5P2 strongly inhibits the growth and metastasis of breast and pancreatic tumor. Compared to mice carrying wild type breast tumor, mice carrying PIPKIgamma-depleted tumor showed significantly longer life span and much less recurrence following the removal of primary tumor. Consistently, in breast and pancreatic cancer patients, higher level of phosphorylated PIPKIgamma significantly correlates with higher tumor grade and worse prognosis. These results strongly indicate that PIPKIgamma can be a promising drug target for tumor treatment. In this context, we developed a small molecule screen system to look for small molecule inhibitors against PIPKIgamma. In the future, we will determine how PIPKIgamma and PtdIn4,5P2 coordinate with other proteins to influence the initiation and progression of breast and pancreatic cancer. More importantly, we will actively evaluate the clinical value of our findings to the practice toward these cancers.
