Synthetic Polyamine BPA‐C8 Inhibits TGF‐β1‐Mediated Conversion of Human Dermal Fibroblast to Myofibroblasts and Establishment of Galectin‐1‐Rich Extracellular Matrix in Vitro |
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Authors: | Dr. Alžběta Mifková Dr. Ondřej Kodet Dr. Pavol Szabo Dr. Jan Kučera Dr. Barbora Dvořánková Dr. Sabine André Dr. Girish Koripelly Prof. Dr. Hans‐Joachim Gabius Prof. Dr. Jean‐Marie Lehn Prof. Dr. Karel Smetana Jr. |
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Affiliation: | 1. Institute of Anatomy, Charles University, 1st Faculty of Medicine, U Nemocnice 3, 128 00 Prague (Czech Republic);2. Department of Otorhinolaryngology and Head and Neck Surgery, Charles University, 1st Faculty of Medicine, V úvalu 5, 150 00 Prague (Czech Republic);3. Department of Dermatovenereology, Charles University, 1st Faculty of Medicine, U Nemocnice 2, 128 08 Prague (Czech Republic);4. Institute of Physiological Chemistry, Ludwig‐Maximilians‐University Munich, Faculty of Veterinary Medicine, Veterin?rstrasse 13, 80539 Munich (Germany);5. Institut de Sciences et d'Ingénierie Supramoléculaires (ISIS), University of Strasbourg, 8 allée Gaspard Monge, 67000 Strasbourg (France) |
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Abstract: | Cancer‐associated fibroblasts (CAFs) play a role in the progression of malignant tumors. They are formed by conversion of fibroblasts to smooth muscle α‐actin‐positive (SMA‐positive) myofibroblasts. Polyamines are known to change the arrangement of the actin cytoskeleton by binding to the anionic actin. We tested the effect of the synthetic polyamine BPA‐C8 on the transition of human dermal fibroblasts to myofibroblasts induced either by TGF‐β1 alone or by TGF‐β1 together with adhesion/growth‐regulatory galectin‐1. Pre‐existing CAFs, myofibroblasts from pancreatitis, and rat smooth muscle cells were also exposed to BPA‐C8. BPA‐C8 impaired myofibroblast formation from activated fibroblasts, but it had no effect on cells already expressing SMA. BPA‐C8 also reduced the occurrence of an extracellular matrix around the activated fibroblasts. The reported data thus extend current insights into polyamine activity, adding interference with tumor progression to the tumor‐promoting processes warranting study. |
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Keywords: | actin cancer galectin polycations tenascin |
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