(7月11日)Mass spectrometry-based metabolomics explores tumor metabolism
新闻类型:学术活动  阅读次数:  发布时间:2019-07-04

报告题目:Mass spectrometry-based metabolomics explores tumor metabolism

报告人:林树海 教授

时间:2019年7月11日(周四),下午3:00

单位:厦门大学生命科学学院

地点:福州大学,实验南楼301

个人简介:

林树海博士现任厦门大学生命科学学院教授、课题组长,中国医师协会癌症代谢与治疗委员会委员、中国抗癌协会肿瘤代谢委员会委员、中国细胞生物学细胞代谢分会理事、中国生物物理学会代谢组学分会理事。本科毕业于广州中医药大学,硕士毕业于中山大学,博士毕业于香港浸会大学,曾在香港浸会大学化学系任研究助理教授。有超过10年从事质谱技术、代谢组学和肿瘤代谢研究的经历,已在Nature Communications(两篇)、Cancer Research、Theranostics、Cell Death & Disease等国际学术期刊上发表40余篇论文, H-index 26。课题组主要发展质谱新技术新方法及其应用研究,包括代谢组学,稳定同位素标记的代谢流分析和质谱流式细胞分析,特别是开展肿瘤微环境的代谢模式与重编程机制。目前正在进行的研究项目基本上整合了分析化学、生物化学、分子细胞生物学,乃至数学建模。

摘要:

One of the biggest hurdles for the development of metabolism-targeted therapies is to identify the responsive tumor subsets. However, the metabolic vulnerabilities for most human cancers remain unclear. Establishing the link between metabolic signatures and the oncogenic alterations of receptor tyrosine kinases (RTK), the most well-defined cancer genotypes, may precisely direct metabolic intervention to broad cancer patients. By integrating metabolomics and transcriptomics, we herein show that oncogenic RTKs activation causes distinct metabolic preference. EGFR activation branches glycolysis to the serine synthesis for biosynthesis and redox homeostasis whereas FGFR addition recycles lactate to fuel oxidative phosphorylation for energy generation. Genetic alterations of EGFR and FGFR stratify the responsive tumor subsets to pharmacological inhibitors shutting down serine and lactate fluxes, respectively. Together, this study provides the molecular link between cancer genotypes and metabolic dependency for patient stratification in metabolism-targeted therapies. 

I will also share another story about the metabolic enzyme transketolase (TKT) in liver injury and cancer initiation. We found that loss of TKT not only retards liver tumor growth but also protects the liver from DNA damage. Indeed, loss of TKT causes the accumulation of ribose 5-phosphate and enhanced levels of nucleotides. These results suggest that the metabolic reprogramming functions the cellular fate and alters tumorigenesis process.   

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