Antithetical NFATc1-Sox2 and p53-miR200 signaling networks govern pancreatic cancer cell plasticity.

@article{Singh2015AntitheticalNA,
  title={Antithetical NFATc1-Sox2 and p53-miR200 signaling networks govern pancreatic cancer cell plasticity.},
  author={Shiv K. Singh and N Chen and Elisabeth Hessmann and Jens T. Siveke and Marlen Lahmann and Garima R. Singh and Nadine Voelker and Sophia Vogt and Irene Esposito and Ansgar Schmidt and Cornelia A Brendel and Thorsten Stiewe and Jochen Gaedcke and Marco Mernberger and Howard C. Crawford and William R. Bamlet and Jin-San Zhang and Xiao-kun Li and Thomas C. Smyrk and Daniel D Billadeau and Matthias Hebrok and Albrecht Neesse and Alexander O. Koenig and Volker Ellenrieder},
  journal={The EMBO journal},
  year={2015},
  volume={34 4},
  pages={517-30}
}
In adaptation to oncogenic signals, pancreatic ductal adenocarcinoma (PDAC) cells undergo epithelial-mesenchymal transition (EMT), a process combining tumor cell dedifferentiation with acquisition of stemness features. However, the mechanisms linking oncogene-induced signaling pathways with EMT and stemness remain largely elusive. Here, we uncover the inflammation-induced transcription factor NFATc1 as a central regulator of pancreatic cancer cell plasticity. In particular, we show that NFATc1… CONTINUE READING