Abstract
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.
Highlights
We showed that NPM1 was up-regulated in Pancreatic ductal adenocarcinoma (PDAC), which indicated a poor prognosis
NPM1 is a multifaceted nucleolar protein that is involved in several cellular processes, including ribosome biogenesis [1], nucleo cytoplasmic transport, centrosome duplication [2, 3], embryonic development [4], histone chaperone function, and transcriptional regulation [5, 6]
Some groups have reported that NPM1 gene mutations are typically absent in common solid cancers [9], which suggests that the NPM1 mutation may not play a role in the tumorigenesis of common solid cancers
Summary
NPM1 (nucleophosmin or B23) is a multifaceted nucleolar protein that is involved in several cellular processes, including ribosome biogenesis [1], nucleo cytoplasmic transport, centrosome duplication [2, 3], embryonic development [4], histone chaperone function, and transcriptional regulation [5, 6]. NPM1 promotes aerobic glycolysis and tumor progression in patients with pancreatic cancer by inhibiting FBP1. We demonstrated that NPM1 ex pression is up-regulated in pancreatic ductal adeno carcinomas, while elevated expression in tumor tissues www.impactjournals.com/oncotarget may be linked to a poorer prognosis. Knock-downs of NPM1 in pancreatic cancer cell lines likely impair glucose uptake and lactate production.
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