IL-6R/STAT3/miR-34a feedback loop promotes EMT-mediated colorectal cancer invasion and metastasis
نویسندگان
چکیده
1Experimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-University Munich, Munich, Germany. 2Institute of Molecular Immunology, Klinikum Rechts der Isar, Technical University Munich, Munich, Germany. 3Institute for Multiple Sclerosis Research and Department of Neuroimmunology, Gemeinnützige Hertie-Stiftung, and University Medical Center Göttingen, Göttingen, Germany. 4Institute of Pathology, Ludwig-Maximilians-University Munich, Munich, Germany. 5Institute of Pathology and 6Department of General Surgery, Klinikum Rechts der Isar, Technical University Munich, Munich, Germany. 7Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt, Germany. 8German Cancer Consortium (DKTK), Heidelberg, Germany. 9German Cancer Research Center (DKFZ), Heidelberg, Germany.
منابع مشابه
Soluble IL6R represents a miR-34a target: potential implications for the recently identified IL-6R/STAT3/miR-34a feed-back loop
We previously reported that IL-6R, STAT3 and miR-34a form a positive feedback-loop, which promotes epithelial to mesenchymal transition (EMT), invasion, and metastasis of colorectal cancer (CRC) [1]. In that study only the membrane-bound form of the IL-6R was shown to be repressed by miR-34a. Here, we show that also the mRNA encoding the soluble IL6R (s-IL-6R) is directly targeted and repressed...
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