报告题目：Inhibition of MEK Signaling Alleviates Tumor-induced Host Wasting
报告人：宋威 博士
主持人：叶升 教授
时 间：2017年4月11日（周二）下午4点
地 点：纳米楼457报告厅
报告人简介：
宋威博士2005年获武汉大学生物技术学士学位，2010年获中国科学院上海生命科学研究院生物化学与分子生物学博士学位。2011年至今在美国哈佛医学院遗传学系进行博士后研究，多次作为特邀报告人参加国际学术会议。
宋威博士致力于研究在癌症恶病质的背景下果蝇和哺乳动物代谢紊乱的分子机制。迄今以第一作者在Cell Metabolism、Cell Reports等发表数篇研究论文。
讲座摘要：
Interactions between tumors and host tissues play essential roles in tumor-induced systemic wasting or cancer cachexia, including muscle wasting and lipid loss. However, the pathogenic molecular mechanisms of wasting are still poorly understood. Using a fly tumor-induced organ wasting model, we demonstrate that MEK signaling is aberrantly activated in the fat and muscle tissues of flies bearing gut ykiact tumors. Genetic activation of MEK/ERK cascade specifically in wild-type muscles and fat body results in muscle wasting and lipid loss, respectively. Strikingly, through either administrating drug after tumor formation or generating drug-resistant ykiact-gut tumor, feeding ykiact tumor-bearing flies with MEK/ERK inhibitors significantly suppresses systemic MEK activation and abolishes cachectic-like phenotypes, including muscle wasting, lipid loss, hyperglycemia and mortality, without affecting tumor progression. MEK activation and systemic wasting in host tissues is regulated by PDGF- and VEGF-related factor 1 (Pvf1) produced by ykiact tumors. Our results demonstrate the essential roles of ERK activation in tumor-induced wasting and indicate that MEK/ERK inhibitors could be used for treatment of cancer cachexia. In support of this, beneficial effects were also observed in mammalian wasting models, as MEK/ERK inhibitors improves lipid loss in adipocytes and muscle atrophy induced by conditioned medium from C26 cachectic cancer cells.
