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PLoS One ; 10(11): e0142527, 2015.
Article in English | MEDLINE | ID: mdl-26562785

ABSTRACT

The cysteine protease cathepsin B has been causally linked to progression and metastasis of breast cancers. We demonstrate inhibition by a dipeptidyl nitrile inhibitor (compound 1) of cathepsin B activity and also of pericellular degradation of dye-quenched collagen IV by living breast cancer cells. To image, localize and quantify collagen IV degradation in real-time we used 3D pathomimetic breast cancer models designed to mimic the in vivo microenvironment of breast cancers. We further report the synthesis and characterization of a caged version of compound 1, [Ru(bpy)2(1)2](BF4)2 (compound 2), which can be photoactivated with visible light. Upon light activation, compound 2, like compound 1, inhibited cathepsin B activity and pericellular collagen IV degradation by the 3D pathomimetic models of living breast cancer cells, without causing toxicity. We suggest that caged inhibitor 2 is a prototype for cathepsin B inhibitors that can control both the site and timing of inhibition in cancer.


Subject(s)
Cathepsin B/antagonists & inhibitors , Cysteine Proteinase Inhibitors/pharmacology , Ruthenium Compounds/pharmacology , Tumor Microenvironment/drug effects , Biocatalysis/drug effects , Cathepsin B/metabolism , Cell Culture Techniques , Cell Line, Tumor , Cell Survival/drug effects , Collagen Type IV/metabolism , Cysteine Proteinase Inhibitors/chemistry , Diagnostic Imaging/methods , Dose-Response Relationship, Drug , Humans , Light , Microscopy, Confocal , Molecular Structure , Photochemical Processes/radiation effects , Proteolysis/drug effects , Ruthenium Compounds/chemistry , Triple Negative Breast Neoplasms/metabolism , Triple Negative Breast Neoplasms/pathology
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