Involvement of the interferon signaling pathways in pancreatic cancer cells

Mariko Fujisawa, Tatsuo Kanda, Toshikatsu Shibata, Reina Sasaki, Ryota Masuzaki, Naoki Matsumoto, Kazushige Nirei, Hiroo Imazu, Kazumichi Kuroda, Masahiko Sugitani, Tadatoshi Takayama, Mitsuhiko Moriyama

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


Background/Aim: To examine interferon (IFN) signaling pathways in human pancreatic cancer cells and their therapeutic application for pancreatic ductal adenocarcinoma (PDAC). Materials and Methods: We examined the effects of IFNα on cytotoxicity, migration, as well as on the levels of tolllike receptor (TLR) signaling pathway-associated genes expression in pancreatic cancer cells. We also examined the additive effects of IFNα and poly(I-C) on tyrosine kinase inhibitor (TKI)-induced cytotoxicity. We performed transcriptome analysis (RNA-Seq) of clinical samples and compared the profile between pancreatic intraepithelial neoplasias (PanINs) and PDACs. Results: IFNα suppressed cell viability and cell migration, and affected TLR signaling pathways, in pancreatic cancer cells. TLR3 is one of the potential genes involved in IFNtreated pancreatic cancer cells. Furthermore, similar to IFN, extracellular addition of poly(I-C) enhanced TKI-induced cytotoxicity in pancreatic cancer cells. RNA-Seq analysis demonstrated that IFN signaling is one of the potential pathways involved in the progression of PanIN to PDAC. Conclusion: IFN signaling may be involved in the development of PDAC. Treatments that target the IFN and TLR3 signaling pathways may be therapeutic options against PDAC.

Original languageEnglish
Pages (from-to)4445-4455
Number of pages11
JournalAnticancer Research
Issue number8
Publication statusPublished - Aug 2020


  • Interferon
  • Pancreatic cancer
  • RNA-Seq
  • TKI
  • Toll-like receptor


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