Neutrophil elastase selectively kills cancer cells and attenuates tumorigenesis

Cancer cell genetic variability and similarity to host cells have stymied development of broad anti-cancer therapeutics. Our innate immune system evolved to clear genetically diverse pathogens and limit host toxicity; however, whether/how innate immunity can produce similar effects in cancer is unkn...

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Veröffentlicht in:	Cell 2021-06, Vol.184 (12), p.3163-3177.e21
Hauptverfasser:	Cui, Chang, Chakraborty, Kasturi, Tang, Xu Anna, Zhou, Guolin, Schoenfelt, Kelly Q., Becker, Kristen M., Hoffman, Alexandria, Chang, Ya-Fang, Blank, Ariane, Reardon, Catherine A., Kenny, Hilary A., Vaisar, Tomas, Lengyel, Ernst, Greene, Geoffrey, Becker, Lev
Format:	Artikel
Sprache:	eng
Schlagworte:	Allosteric Regulation - drug effects Animals cancer Carcinogenesis - drug effects Carcinogenesis - pathology CD8-Positive T-Lymphocytes - immunology CD95 Cell Death - drug effects Cell Line, Tumor Cell Proliferation - drug effects Eosinophil Cationic Protein - metabolism fas Receptor - chemistry fas Receptor - metabolism histone H1 Histones - metabolism Humans Leukocyte Elastase - metabolism Mice Neoplasms - enzymology Neoplasms - immunology Neoplasms - pathology neutrophil estate neutrophils Neutrophils - drug effects Neutrophils - enzymology Pancreatic Elastase - metabolism Protease Inhibitors - pharmacology Protein Domains Protein Isoforms - metabolism Proteolysis - drug effects Secretory Leukocyte Peptidase Inhibitor - metabolism Swine therapeutics tumor immunology
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