Transcription factor NFAT5 contributes to the glycolytic phenotype rewiring and pancreatic cancer progression via transcription of PGK1

• DOI: 10.1038/s41419-019-2072-5
• Publication Date: 2019-12-11T13:05:58Z
• Authors: Yongsheng Jiang; Ruizhe He; Yuhong Jiang; Dejun Liu; Lingye Tao; Minwei Yang; Chaoyi Lin; Yang Shen; Xueliang Fu; Jianyu Yang; Jiao Li; Yanmiao Huo; Rong Hua; Wei Liu; Junfeng Zhang; Baiyong Shen; Zhigang Zhang; Yongwei Sun
• Keywords: Phosphoglycerate kinase; Warburg Effect

Abstract Hypoxia and the hypovascular tumor microenvironment are major hallmarks of pancreatic ductal adenocarcinoma (PDAC), in which glycolysis is great importance to survival proliferation. There little research regarding role Nuclear Factor Activated T Cells 5 (NFAT5) relation carcinoma. Here, we explored impact NFAT5 on biological behavior PDAC underlying mechanism. We demonstrated that was highly expressed related poorer prognosis. Knockdown lead impaired proliferation cells caused by an aberrant Warburg effect. Mechanically, phosphoglycerate kinase 1 (PGK-1), first enzyme generating ATP glycolysis, verified as a target gene NFAT5. Over-expression PGK1 compromised oncological knockdown both vitro vivo. Clinical samples underwent positron emission tomography-computed tomography (PET-CT) examination KrasG12D/+/Trp53R172H/+/Pdx1-Cre (KPC) mice were collected support our conclusion.