果糖-1，6-二磷酸酶1（FBP1）作为糖异生途径的限速酶参与细胞内葡萄糖代谢的调控。研究显示FBP1在胰腺癌中表达下调并且参与阻遏胰腺癌进展,但FBP1是如何抑制胰腺癌进展的分子机制目前尚不清楚。原癌基因 c-Myc 在胰腺癌中高表达但受多种因素的调控。我们前期实验结果发现在胰腺癌细胞系 PANC-1 中，敲低 FBP1 后 c-Myc 蛋白水平升高，而过表达 FBP1 后 c-Myc 蛋白水平下降。因此我们推测 FBP1 参与 c-Myc 在胰腺癌细胞中的调控。本项目拟在前期工作基础上系统地研究 FBP1 下调 c-Myc 的分子机制以及明确 FBP1 能否通过下调 c-Myc 影响胰腺癌进展，最终为揭示FBP1新的抑癌机制和为探寻胰腺癌防治的分子靶点提供理论依据。

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancer types worldwide.Fructose-1,6-bisphosphatase (FBP1) a key enzyme in gluconeogenesis, is down-regulated in PDAC. We demonstrated that FBP1 functioned as a tumor suppressor and inhibited PDAC progression. Oncoprotein c-Myc is up-regulated in PDAC. Here, we showed that knockdown of FBP1 up-regulated c-Myc protein levels while over-expressed of FBP1 decreased c-Myc protein levels in PANC-1 cells. The mechanism of FBP1 down-regulation of c-Myc is still unclear. The purpose of this project is to explore the mechanism of down-regulation of c-Myc mediated by FBP1. Most importantly, we intend to explore whether FBP1 could opposes PDAC progression via down-regulation of c-Myc and develop new therapeutic strategies to treat pancreatic cancer.