system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Blotting, Western, Butadienes, Carcinoma, Squamous Cell, Cell Line, Tumor, Cytoprotection, Electrophoresis, Polyacrylamide Gel, Enzyme Inhibitors, Enzyme-Linked Immunosorbent Assay, Extracellular Signal-Regulated MAP Kinases, Humans, Hydrogen Peroxide, Immunohistochemistry, MAP Kinase Signaling System, Nitriles, Radiation Tolerance, Reactive Oxygen Species, Up-Regulation, Vascular Endothelial Growth Factor A.
user
Does reactive oxygen species activation of MAPK pathway result in VEGF upregulation as an undesired irradiation response? Context: Radioresistance limits the effectiveness of radiotherapy in head and neck squamous cell carcinoma. We previously demonstrated post-radiogenic mitogen-activated protein kinase (MAPK) pathway activation and vascular endothelial growth factor (VEGF) release resulting in reduced tumor cell response. Here, we examined the association of this mechanism with the induction of reactive oxygen species (ROS) under irradiation (IR). Intracellular ROS after IR were measured. We modeled radiation-induced ROS by exposure of two SCC lines to H2 O2 and evaluated the impact of irradiation and ROS on ERK phosphorylation by Western blot, immunohistochemistry, and ELISA. We found elevated pERK levels after treatment with IR and H2 O2 , which could be distinctly suppressed by U0126. Immunohistochemistry and ELISA revealed increased intracellular VEGF levels after H2 O2 application.
assistant
Our data show that irradiation-induced ROS activate the MAPK pathway and release of VEGF. As VEGF is known to be released after cellular distress resulting in cytoprotection, the described mechanism is potentially of importance for therapy success. Final Decision: yes