NPM1 activates metabolic changes by inhibiting FBP1 while promoting the tumorigenicity of pancreatic cancer cells.
NPM1 activates metabolic changes by inhibiting FBP1 while promoting the tumorigenicity of pancreatic cancer cells.
复制标题
NPM1 通过抑制 FBP1 来激活代谢变化，同时促进胰腺癌细胞的致瘤性。
DOI：
10.18632/oncotarget.4167
复制
发表时间：
2015-08-28
期刊：
影响因子：
--
通讯作者：
Peng C
中科院分区：
文献类型：
--
作者：
Zhu Y;Shi M;Chen H;Gu J;Zhang J;Shen B;Deng X;Xie J;Zhan X;Peng C
核磷蛋白（NPM 1）在许多恶性肿瘤中激活癌症的发展和进展。然而，NPM 1在胰腺癌中的调节作用和潜在机制尚不清楚。在这项研究中，我们发现NPM 1在PDAC中上调，这表明预后不良。我们还发现NPM 1可以刺激胰腺癌细胞的有氧糖酵解并抑制果糖-1，6-二磷酸酶1（FBP 1）。恢复FBP 1表达部分逆转了NPM 1的促肿瘤作用，而PDAC组织中FBP 1的缺失表明预后较差。总之，NPM 1通过抑制FBP 1促进胰腺癌患者的有氧糖酵解和肿瘤进展。
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 NPM1could 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.