NRF2 Promotes Tumor Maintenance by Modulating mRNA Translation in Pancreatic Cancer

نویسندگان

  • Iok In Christine Chio
  • Seyed Mehdi Jafarnejad
  • Mariano Ponz-Sarvise
  • Youngkyu Park
  • Keith Rivera
  • Wilhelm Palm
  • John Wilson
  • Vineet Sangar
  • Yuan Hao
  • Daniel Öhlund
  • Kevin Wright
  • Dea Filippini
  • Eun Jung Lee
  • Brandon Da Silva
  • Christina Schoepfer
  • John Erby Wilkinson
  • Jonathan M. Buscaglia
  • Gina M. DeNicola
  • Herve Tiriac
  • Molly Hammell
  • Howard C. Crawford
  • Edward E. Schmidt
  • Craig B. Thompson
  • Darryl J. Pappin
  • Nahum Sonenberg
  • David A. Tuveson
چکیده

Pancreatic cancer is a deadly malignancy that lacks effective therapeutics. We previously reported that oncogenic Kras induced the redox master regulator Nfe2l2/Nrf2 to stimulate pancreatic and lung cancer initiation. Here, we show that NRF2 is necessary to maintain pancreatic cancer proliferation by regulating mRNA translation. Specifically, loss of NRF2 led to defects in autocrine epidermal growth factor receptor (EGFR) signaling and oxidation of specific translational regulatory proteins, resulting in impaired cap-dependent and cap-independent mRNA translation in pancreatic cancer cells. Combined targeting of the EGFR effector AKT and the glutathione antioxidant pathway mimicked Nrf2 ablation to potently inhibit pancreatic cancer ex vivo and in vivo, representing a promising synthetic lethal strategy for treating the disease.

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عنوان ژورنال:
  • Cell

دوره 166  شماره 

صفحات  -

تاریخ انتشار 2016