Research Papers:

NPM1 activates metabolic changes by inhibiting FBP1 while promoting the tumorigenicity of pancreatic cancer cells

Yi Zhu _, Minmin Shi, Hao Chen, Jiangning Gu, Jiaqiang Zhang, Baiyong Shen, Xiaxing Deng, Junjie Xie, Xi Zhan and Chenghong Peng

PDF  |  HTML  |  Supplementary Files  |  How to cite  |  Order a Reprint

Oncotarget. 2015; 6:21443-21451. https://doi.org/10.18632/oncotarget.4167

Metrics: PDF 1694 views  |   HTML 1867 views  |   ?  


Yi Zhu1,*, Minmin Shi2,*, Hao Chen1,2, Jiangning Gu1, Jiaqiang Zhang1, Baiyong Shen1,2, Xiaxing Deng1,2, Junjie Xie1, Xi Zhan1,2, Chenghong Peng1,2

1Department of Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China

2Research Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China

*These authors have contributed equally to this work

Correspondence to:

Hao Chen, e-mail: haochendr@126.com

Chenghong Peng, e-mail: chhpeng@188.com

Keywords: pancreatic ductal adenocarcinoma, NPM1, FBP1, warburg effect

Received: March 30, 2015     Accepted: May 23, 2015     Published: June 05, 2015


The nucleophosmin (NPM1) activates cancer development and progression in many malignant tumors. However, the regulatory role and underlying mechanisms of NPM1 in pancreatic cancer are unknown. In this study, we showed that NPM1 was up-regulated in PDAC, which indicated a poor prognosis. We also identified NPM1 could stimulate aerobic glycolysis and repress fructose-1, 6-bisphosphatase 1 (FBP1) in pancreatic cancer cells. Restoring FBP1 expression partially reversed the tumor-promoting effects of NPM1, while the loss of FBP1 in PDAC tissues was indicative of a poorer prognosis. In sum, NPM1 promotes aerobic glycolysis and tumor progression in patients with pancreatic cancer by inhibiting FBP1.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 4167