报告题目：Non-metabolic Funtions of M2 Isoform of Pyruvate Kinase in EGFR-promoted Brain Tumor Development

报告人：   Weiwei Yang, Ph.D.

                 Postdoctoral fellow

                 The University of Texas MD Anderson Cancer Center  

主持人： 冯新华 教授

时   间： 2012年9月21日（星期五）下午4：00

地   点： 医学院综合楼205报告厅

Abstract：

The embryonic enzyme pyruvate kinase M2 (PKM2) has a well-established role in metabolism and is highly expressed in human cancers. We reports that PKM2 has important non-metabolic functions in cancer formation. Basically, PKM2 contributes directly to gene transcription for cell growth. In response to epidermal growth factor (EGF), PKM2 moves to cell nucleus and binds to beta-catenin that has been phosphorylated at Y333 by c-Src. This binding is essential for beta-catenin activation and expression of downstream gene cyclin D1. This new discovered way to regulated beta-catenin is independent of the Wnt signaling pathway previously know to activate beta-catenin. In addition, levels of beta-catenin phosphorylation and PKM2 in the nucleus are correlated with brain tumor malignancy and prognosis and might serve as biomarkers for customized treatment with Src inhibitors.