肿瘤代谢重编程是癌症的核心特征，被认为是胶质瘤发病机制的中心驱动力。然而，目前国内外尚无有效干预肿瘤代谢的有效策略和药物。我们在国际上首次发现1，6-二磷酸果糖（FBP）对胶质瘤和其它癌细胞具有杀伤作用，其整体抗胶质瘤药效优于治疗胶质瘤国际金标药替莫唑胺，可全面逆转肿瘤特征性代谢，有望成为又一个老药新用的典范。本研究围绕核心科学假说“FBP可消除胶质瘤中乙酰辅酶A乙酰化目标蛋白介导的调节肿瘤特征性代谢、促癌信号通路和促癌基因表达的核心枢纽作用”，在细胞和整体水平，采用多学科交叉的技术方法，研究FBP逆转胶质瘤线粒体代谢酶乙酰化特征、胞浆和核中多种类型功能蛋白乙酰化、Ac-CoA隔室分布与产生的作用及相关作用机制。研究结果可揭示FBP 对抗癌代谢特征的新作用，阐明FBP逆转肿瘤特征代谢的独特分子机制，奠定其作为新类型抗癌药物的科学基础，并为针对癌代谢特征研发新类型抗癌药提供新思路。

Caner metabolism reprogramming is a core hallmark of cancer and proposed as a central driving force of glioma pathogenesis. However, there is no effective strategy or drug for the intervention of tumor metabolism at present. For the first time, we found that fructose-1,6-bisphosphate (FBP) can kill glioblastoma and other types of cancer cells and its in vivo anti-glioblastoma efficacy is better than that of temozolomide，a gold standard drug for glioblastoma. FBP is able to comprehensively reverse tumor metabolism and expected to become another good example of new uses of old drugs. To date, there are no any kinds of anti-tumor activity substances similar to FBP. This study focuses on the core scientific hypothesis “FBP can eliminate the key role of Ac-CoA acetylated target proteins in regulating tumor metabolism, promoting cancer signaling pathway and oncogenic gene expression”. By using a variety of interdisciplinary technical methods, we will investigate the potential effects and underlying mechanisms of FBP against acetylation of mitochondrial metabolic enzymes, various functional proteins in cytoplasm and nucleus, and compartment distribution and production of Ac-CoA in glioblastoma cells at both cellular and whole body levels. The results of this study will reveal new actions of FBP against cancer metabolism hallmarks, elucidate the unique molecular mechanism of FBP in reversing tumor metabolism, lay the scientific foundation for FBP as a new class of anticancer drugs, and provide new ideas for the development of new types of anticancer drugs through targeting cancer specific metabolism.