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• W2070460611 abstract "<h3>Objective</h3> The lysosomal protease cathepsin B is upregulated in human pancreatic ductal adenocarcinoma (PDA) and represents a potential therapeutic target. Loss of cathepsin B delays tumour progression in mouse models of islet, mammary and intestinal carcinoma and decreases invasion and metastasis. This study examines the role of cathepsin B in the initiation, progression and metastasis of PDA. <h3>Methods</h3> Cathepsin B germline knockout mice were crossed with animals expressing an endogenous <i>Kras^G12D</i> allele in the pancreas, and mice were aged to evaluate the role of cathepsin B in pancreatic intraepithelial neoplasia (PanIN). A survival study was also performed with mice carrying an additional heterozygous conditional <i>Trp53^R172H</i> allele. Cell lines derived from tumours were used to investigate the role of cathepsin B in vitro, and subcutaneous allografts investigated the cell autonomous and non-cell autonomous roles of cathepsin B in pancreatic cancer. <h3>Results</h3> Constitutive cathepsin B loss resulted in delayed progression of both PanIN and PDA and a significant survival advantage in mice. Cathepsin B-deficient PDA cells and PanIN showed decreased proliferation and mitogen-activated protein (MAP) kinase signalling. The reconstitution of deficient cells with cathepsin B reversed these findings, which correlated with decreased levels of the active forms of the related protease cathepsin L. Conversely, acute ablation of cathepsin L activated the MAP kinase cascade in PDA cells. <h3>Conclusions</h3> These results confirm that cathepsin B plays an important cell autonomous role in the progression of PDA and suggest that the regulation of cathepsin L by cathepsin B may be a means of stimulating cell proliferation in neoplasia." @default.
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• W2070460611 date "2011-12-09" @default.
• W2070460611 modified "2023-10-15" @default.
• W2070460611 title "Cathepsin B promotes the progression of pancreatic ductal adenocarcinoma in mice" @default.
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• W2070460611 doi "https://doi.org/10.1136/gutjnl-2011-300850" @default.
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