Injured tissues favor cancer cell implantation via fibrin deposits on scar zones
| Autor: | Djedjiga Abdelhamid, Massoud Mirshahi, Shahsoltan Mirshahi, Iman Al dybiat, Meriem Belalou, Marc Pocard, Matti Ullah, Jeannette Soria, Shahid Shah |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Cancer Research Plasmin medicine.medical_treatment Cell Culture Techniques Fluorescent Antibody Technique HMCs human mesothelial cells Mice 0302 clinical medicine DMEM dulbecco's Modified Eagle Medium Aprotinin PCI peritoneal Cancer Index uPA urokinase plasminogen activator PA plasminogen activator biology Chemistry ELISA enzyme-linked immunosorbent assay lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens 030220 oncology & carcinogenesis CTRL control qPCR quantitative polymerase chain reaction Female Peritoneum PAR protease-activated receptors medicine.drug Original article NETs neutrophil extracellular traps SEM scanning electron microscope CT26 mouse colon cancer cell line PBS phosphate-buffered saline lcsh:RC254-282 Fibrin Cicatrix 03 medical and health sciences Thrombin Cell Line Tumor Fibrinolysis Cell Adhesion medicine Animals Humans ATCC American Type Culture Collection Fibrin degradation product Cancer medicine.disease PAI-1 plasminogen activator inhibitor Molecular biology tPA tissue plasminogen activator Disease Models Animal 030104 developmental biology Cancer cell biology.protein PFA paraformaldehyde Neoplasm Transplantation |
| Zdroj: | Neoplasia: An International Journal for Oncology Research, Vol 22, Iss 12, Pp 809-819 (2020) Neoplasia (New York, N.Y.) |
| ISSN: | 1476-5586 |
| Popis: | Aim Evaluation of fibrin role on cancer cells implantation in injured tissues and studying the molecular mechanism of cancer cell interaction with the peritoneal damage. Material and methods Mouse colon cancer (CT26) and human mesothelial cells (HMCs) were used. CT26 cells were implanted on injured peritoneal zones. Icodextrin was used as a lubricant. For in vitro studies, fibrin clots from human plasma were used. The cell-fibrin interaction was observed by optical, electronic, and confocal microscopies. Aprotinin was used as a plasmin inhibitor. Hemostasis impact quantified by (1) the fibrin degradation product D-Dimer and PAR expression in HMCs; (2) the expression of plasminogen activator (PA) and its inhibitor (PAI-1) in cancer cells by qPCR and in supernatants through ELISA after in vitro HMC incubation with 2U of thrombin for 24 h. Results (i) Cancer cell lines were adhered and implanted into the wound area in vivo in both the incision and peeling zones of the peritoneum and on the fibrin network in vitro. (ii) Icodextrin significantly inhibited cancer nodule formation in the scar and the incision or peritoneal damaged zones after surgery. (iii) In in vitro studies, cancer cell interaction with the fibrin clot generated a lysed area, causing an increase in plasmin-dependent fibrinolysis measured by D-dimer levels in the supernatants that was inhibited by aprotinin. (iv) Aprotinin inhibited cell-fibrin interaction and invasion. (v) Thrombin upregulates PAI-1 and downregulates PA expression in HMC. Conclusion Injured tissues favor cancer cell implantation through generated fibrin. Fibrin-cancer cells adhesion can be inhibited by icodextrin. |
| Databáze: | OpenAIRE |
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