Loss of fibulin-5 binding to beta1 integrins inhibits tumor growth by increasing the level of ROS

Tumor survival depends in part on the ability of tumor cells to transform the surrounding extracellular matrix (ECM) into an environment conducive to tumor progression. Matricellular proteins are secreted into the ECM and impact signaling pathways that are required for pro-tumorigenic activities suc...

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Veröffentlicht in:	Disease models & mechanisms 2010-05, Vol.3 (5-6), p.333-342
Hauptverfasser:	Schluterman, Marie K, Chapman, Shelby L, Korpanty, Grzegorz, Ozumi, Kiyoshi, Fukai, Tohru, Yanagisawa, Hiromi, Brekken, Rolf A
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antioxidants - pharmacology Antioxidants - therapeutic use Apoptosis - drug effects Cell Line, Tumor Cell Proliferation - drug effects Embryo, Mammalian - cytology Endothelial Cells - drug effects Endothelial Cells - metabolism Endothelial Cells - pathology Extracellular Matrix Proteins - deficiency Extracellular Matrix Proteins - metabolism Fibroblasts - drug effects Fibroblasts - metabolism Fibronectins - metabolism Integrin beta1 - metabolism Mice Neovascularization, Pathologic - drug therapy Neovascularization, Pathologic - pathology Oxidative Stress - drug effects Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Protein Binding - drug effects Reactive Oxygen Species - metabolism Recombinant Proteins - metabolism
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