Inhibition of Nogo-B reduces the progression of pancreatic cancer by regulation NF-KB/GLUT1 and SREBP1 pathways

Pancreatic cancer (PC) is a lethal disease and associated with metabolism dysregulation. Nogo-B is related to multiple metabolic related diseases and types of cancers. However, the role of Nogo-B in PC remains unknown. In vitro , we showed that cell viability and migration was largely reduced in Nogo-B knockout or knockdown cells, while enhanced by Nogo-B overexpression. Consistently, orthotopic tumor and metastasis was reduced in global Nogo knockout mice. Furthermore, we indicated that glucose enhanced cell proliferation was associated to the elevation expression of Nogo-B and nuclear factor K B (NF - K B). While, NF - K B, glucose transporter type 1 (GLUT1) and sterol regulatory element -binding protein 1 (SREBP1) expression was reduced in Nogo-B deficiency cells. In addition, we showed that GLUT1 and SREBP1 was downstream target of NF - K B. Therefore, we demonstrated that Nogo deficiency inhibited PC progression is regulated by the NF- K B/GLUT1 and SREBP1 pathways, and suggested that Nogo-B may be a target for PC therapy.