Renalase is over-expressed and activates STAT3 in pancreatic cancer

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Renalase (RNLS) is a secreted flavoprotein. It is over-expressed by pancreatic cancer and acts as a survival factor blocking apoptosis. Importantly RNLS activates STAT3 and establishes a positive feedback loop whereby STAT3 promotes greater RNLS expression [1].

STAT3 plays a major role in pancreatic cancer [2]. It will be very important to determine through further research the extent to which STAT3 mediates renalase’s pro-cancer effects. A combination of renalase and STAT3 inhibition may prove effective against pancreatic cancer. A STAT3 inhibitor is already in clinical trials [3].

As renalase is secreted it may also serve as a useful diagnostic blood biomarker of pancreatic cancer (See here for pancreatic cancer biomarkers under development). This is certainly worth pursuing as late detection is a major reason for the dismal outcomes of pancreatic cancer patients.


  1. Guo, Xiaojia, Lindsay Hollander, Douglas MacPherson, Ling Wang, Heino Velazquez, John Chang, Robert Safirstein, Charles Cha, Fred Gorelick, and Gary V. Desir. ‘Inhibition of Renalase Expression and Signaling Has Antitumor Activity in Pancreatic Cancer’. Scientific Reports 6 (14 March 2016): 22996. doi:10.1038/srep22996.
  2. Corcoran, R. B., G. Contino, V. Deshpande, A. Tzatsos, C. Conrad, C. H. Benes, D. E. Levy, J. Settleman, J. A. Engelman, and N. Bardeesy. ‘STAT3 Plays a Critical Role in KRAS-Induced Pancreatic Tumorigenesis’. Cancer Research 71, no. 14 (15 July 2011): 5020–29. doi:10.1158/0008-5472.CAN-11-0908.
  3. Hong, David, Razelle Kurzrock, Youngsoo Kim, Richard Woessner, Anas Younes, John Nemunaitis, Nathan Fowler, et al. ‘AZD9150, a next-Generation Antisense Oligonucleotide Inhibitor of STAT3 with Early Evidence of Clinical Activity in Lymphoma and Lung Cancer’. Science Translational Medicine 7, no. 314 (18 November 2015): 314ra185. doi:10.1126/scitranslmed.aac5272.

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