Overexpression of IFN-induced protein with tetratricopeptide repeats 3 (IFIT3) in pancreatic cancer: cellular “pseudoinflammation” contributing to an aggressive phenotype

作者：Hanno Nieß, Peter Čamaj, Ruth Mair, Andrea Renner, Yue Zhao, Carsten Jäckel, Peter J. Nelson, Karl‐Walter Jauch, Christiane J. Bruns · 发表于：Oncotarget · 年份：2014 · DOI：10.18632/oncotarget.2494 · 被引用次数：36 · 研究领域：interferon and immune responses、Ubiquitin and proteasome pathways、NF-κB Signaling Pathways

// Hanno Niess 1 , Peter Camaj 2 , Ruth Mair 1 , Andrea Renner 1 , Yue Zhao 1 , Carsten Jäckel 3 , Peter J. Nelson 3 , Karl-Walter Jauch 1 and Christiane J. Bruns 2 1 Department of Surgery, Medical Center of the Ludwig-Maximilians-University, Campus Grosshadern, Munich, Germany 2 Department of Surgery, Medical Center of the Otto-von-Guericke-University, Magdeburg, Germany 3 Medizinische Klinik und Poliklinik IV, Campus Innenstadt, Klinikum der Universitaet Muenchen, Arbeitsgruppe Klinische Biochemie, Munich, Germany Correspondence: Christiane J. Bruns, email: // Keywords : IFIT, IFIT3, RIG-G, ISG60, SOX9, inflammation, pancreatic cancer, chemotherapy resistance, cytokine expression Received : August 12, 2014 Accepted : September 16, 2014 Published : September 17, 2014 Abstract Inflammation contributes to important traits that cancer cells acquire during malignant progression. Gene array data recently identified upregulation of interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) in aggressive pancreatic cancer cells. IFIT3 belongs to the group of interferon stimulated genes (ISG), can be induced by several cellular stress stimuli and by its tetratricopeptide repeats interacts with a multitude of cellular proteins. Upregulation of IFIT3 was confirmed in the aggressive pancreatic cancer cell line L3.6pl compared with its less aggressive cell line of origin, COLO357FG. Transgenic induction of IFIT3 expression in COLO357FG resulted in greater mass of orthotopi...